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NSYSU
1.
Tsao, Yu-chen.
A Prospective Small Volume Albumin Therapy in Cirrhosis and Spontaneous Bacterial Peritonitis Treatment.
Degree: Master, Institute of Biomedical Sciences, 2008, NSYSU
URL: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0730108-134947 
► In clinical findings, complications are the major cause of death in cirrhotic patients. Among all the complications, ascites is most frequent type. All cirrhotic patients…
(more)
▼ In clinical findings, complications are the major cause of death in
cirrhotic patients. Among all the complications, ascites is most frequent
type. All cirrhotic patients with ascites could develop spontaneous
bacterial peritonitis (SBP). The hospitalized prevalence of SBP was high
(30%) in cirrhotic ascites patients. However, the outcome of cirrhotic
SBP patients has been improved because of using the antibiotics
cephalosporins. Furthermore, treatment with intravenous albumin in
addition to cephalosporins reduced the incidence of renal impairment and
the mortality in SBP patients in a multicentre study. However, other
studies showed that administration of albumin might not work as
effectively as other plasma expanders do. Moreover, administration of
large volume albumin would make the medication very expensive and
might have potential risk of infectious disease, since the therapeutic
albumin is extracted from human plasma. Therefore, to treat patients with
large volume albumin become disputable. In this study, we evaluated the
effects of small volume intravenous albumin with cephalosporins
treatments through monitoring patientsâ renal and hepatic functions and
related inflammatory markers. Results showed that plasma TNF-α, ÎL-6
and ascites endotoxin, TNF-α and IL-6 levels were significantly reduced
in patients treated with cephalosporins plus small volume albumin, but
not in those treated with cephalosporins alone. Also, the combination
therapy of cephalosporins and small volume albumin avoid the
dramatically elevation of plasma and ascites nitric oxide, as well as the
further degree of renal function impairment. The positive results of this
study laid a solid foundation for a large scale investigation.
Advisors/Committee Members: chun%20Hung%22%29&pagesize-30">
Wen-
chun Hung (chair),
Angela Chen (committee member),
Deng-chyang Wu (chair).
Subjects/Keywords: cirrhosis; spontaneous bacterial peritonitis; albumin
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APA (6th Edition):
Tsao, Y. (2008). A Prospective Small Volume Albumin Therapy in Cirrhosis and Spontaneous Bacterial Peritonitis Treatment. (Thesis). NSYSU. Retrieved from http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0730108-134947
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Tsao, Yu-chen. “A Prospective Small Volume Albumin Therapy in Cirrhosis and Spontaneous Bacterial Peritonitis Treatment.” 2008. Thesis, NSYSU. Accessed January 19, 2021.
http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0730108-134947.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Tsao, Yu-chen. “A Prospective Small Volume Albumin Therapy in Cirrhosis and Spontaneous Bacterial Peritonitis Treatment.” 2008. Web. 19 Jan 2021.
Vancouver:
Tsao Y. A Prospective Small Volume Albumin Therapy in Cirrhosis and Spontaneous Bacterial Peritonitis Treatment. [Internet] [Thesis]. NSYSU; 2008. [cited 2021 Jan 19].
Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0730108-134947.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Tsao Y. A Prospective Small Volume Albumin Therapy in Cirrhosis and Spontaneous Bacterial Peritonitis Treatment. [Thesis]. NSYSU; 2008. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0730108-134947
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
NSYSU
2.
Cheng, Yun-Ching.
Evolutionary relationship and cytotoxic mechanism of Taiwan banded krait β-Bungarotoxin's B chains and homologous proteins.
Degree: PhD, Institute of Biomedical Sciences, 2008, NSYSU
URL: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0124108-173924
► β-Bungarotoxin (β-Bgt), a presynaptic phospholipase A2 (PLA2) neurotoxin isolated from the venom of Bungarus multicinctus (Taiwan banded krait), consists of A chain and B chain,…
(more)
▼ β-Bungarotoxin (β-Bgt), a presynaptic phospholipase A2 (PLA2) neurotoxin isolated from the venom of Bungarus multicinctus (Taiwan banded krait), consists of A chain and B chain, cross-linked by an interchain disulfide bond. A chain is structurally homologous with phospholipase A2 (PLA2) enzymes, while the sequence of B chain is homologous to the Kunitz-type protease inhibitor and dendrotoxin. In addition to PLA2 activity, β-Bgt blocked the neurotransmission at the neuromuscular junction by selectively inhibiting certain voltage-sensitive potassium channels. The present studies investigated the B chain of β-bungarotoxin and B chain homologous proteins in evolutionary relationship and cytotoxic mechanism.
Eight A chain cDNAs and three B chain cDNAs have been cloned from B. multicinctus venom glands. Random combination of the A and the B chains should produce a number of β-Bgt isotoxins. There are at least 16 isoforms of β-Bgt were been isolated. Previous studies indicate that A and B chains are encoded separately by different genes, and the A and B chain genes do not originate from a common ancestor. These findings suggest that the intact β-Bgt molecules should be derived from the pairing of A and B chains after their mRNAs are translated. And, our recent studies show that B chain genes and Naja naja atra chymotrypsin inhibitor (NACI) share the same genomic organization and high sequence identity. Alternatively, limited studies on the evolutionary divergence of B chain gene and its homologous have been reported.
In the first part, the structural organization of the genes encoding B2, B4, B5 and B6 chains of β-Bgt are reported. These genes shared virtually identical overall organization with three exons interrupted by two introns in similar positions. On the contrary, intron 1 of these genes had a similar size, a notable variation with the size of intron 2 was observed. It was found that two regions at the second intron of B1 and B2 chains were absent in that of B4, B5 and B6 chains. RT-PCR analyses indicated that Bungarus multicinctus venom gland, heart, liver and muscle expressed the RNA transcripts showing sequence similarity with the intronic segment being deleted in B4, B5 and B6 chain genes. This reflects that the ancestral gene of the intronic segment might insert in multiple loci of B. multicinctus genome. Comparative analyses of B chain genes showed that the protein-coding regions of the exons are more diverse than introns, except for in the signal peptide domain. These results suggest that intron insertions or deletions occur with the evolution of B chains, and that accelerated evolution may diversify the protein-coding sequence of B chain genes same as snake phospholipase A2, neurotoxin and cardiotoxin genes.
The second part is to explore the functional contribution of the two subunits to the toxicity of β-Bgt. β-Bgt was found to induce apoptotic death of SK-N-SH cells via elevating intracellular Ca2+ and intracellular ROS production. Moreover, an activation of p38 MAPK was associated with the…
Advisors/Committee Members: Chun-chang Chang (chair), Long-sen Chang (committee member), chun%20Hung%22%29&pagesize-30">
Wen-
chun Hung (chair).
Subjects/Keywords: β-Bungarotoxin
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MLA ·
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CSE |
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APA (6th Edition):
Cheng, Y. (2008). Evolutionary relationship and cytotoxic mechanism of Taiwan banded krait β-Bungarotoxin's B chains and homologous proteins. (Doctoral Dissertation). NSYSU. Retrieved from http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0124108-173924
Chicago Manual of Style (16th Edition):
Cheng, Yun-Ching. “Evolutionary relationship and cytotoxic mechanism of Taiwan banded krait β-Bungarotoxin's B chains and homologous proteins.” 2008. Doctoral Dissertation, NSYSU. Accessed January 19, 2021.
http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0124108-173924.
MLA Handbook (7th Edition):
Cheng, Yun-Ching. “Evolutionary relationship and cytotoxic mechanism of Taiwan banded krait β-Bungarotoxin's B chains and homologous proteins.” 2008. Web. 19 Jan 2021.
Vancouver:
Cheng Y. Evolutionary relationship and cytotoxic mechanism of Taiwan banded krait β-Bungarotoxin's B chains and homologous proteins. [Internet] [Doctoral dissertation]. NSYSU; 2008. [cited 2021 Jan 19].
Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0124108-173924.
Council of Science Editors:
Cheng Y. Evolutionary relationship and cytotoxic mechanism of Taiwan banded krait β-Bungarotoxin's B chains and homologous proteins. [Doctoral Dissertation]. NSYSU; 2008. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0124108-173924
NSYSU
3.
Liao, Yen-Shun.
Study the functional region involves in targeting of KChIP1 to membrane.
Degree: Master, Institute of Biomedical Sciences, 2008, NSYSU
URL: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0715108-124010
► Potassium channel-interacting protein 1 (KChIP1), a Ca2+ sensor protein, regulates the function of A-type Kv4 potassium channels and increases their cell surface expression. Myristoylation at…
(more)
▼ Potassium channel-interacting protein 1 (KChIP1), a Ca
2+ sensor protein, regulates the function of A-type Kv4 potassium channels and increases their cell surface expression. Myristoylation at the N-terminus of KChIP1 has been suggested to facilitate membrane-binding, but was not sufficient for stable membrane assaociation. The aim of the present study is to investigate whether EF-hand motifs of KChIP1 are crucial for membranal targeting in addition to the N-terminal myristoyl group, and how the membrane association of KChIP1 is influenced by lipid compositions. According to hydropathy profile, EF-hands 3 and 4 of KChIP1 showed highly hydrophobicity. After deleting EF-hands 3 and 4, the altered microenvironment of Trp residue and decreased hydrophobicity were found in truncated KChIP1, but it still maintained α-helix structure. Furthermore, truncated KChIP1 exhibited lower lipid-binding ability, affecting intracellular membrane localization and was almost diminished underlying increasing membrane permeability by digitonin in cells, suggesting that intact EF-hands 3 and 4 may be related to the anchorage of KChIP1 on cellular membrane. KChIP1, but not mutant, specifically bound with phosphatidylserine by lipid binding assay and the FTIR spectra showed the change of α-helix structure by binding lipid large unilamellar vesicles was dependent on phosphatidylserine. Either phosphatidylserine or potassium channels enhanced KChIP1 to form tetramer for targeting to phospholipids by using chemical cross-linking assay. Taken together, our data highly suggest that intact of EF-hands 3 and 4 should structurally and functionally involve in fulfilling the physiological activity of KChIP1.
Advisors/Committee Members: Chun-Chang Chang (chair), Chun%20Hung%22%29&pagesize-30">
Wen-
Chun Hung (chair),
Long-Sen Chang (committee member).
Subjects/Keywords: NCS protein; KChIP1; phosphatidylserine
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APA ·
Chicago ·
MLA ·
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CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Liao, Y. (2008). Study the functional region involves in targeting of KChIP1 to membrane. (Thesis). NSYSU. Retrieved from http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0715108-124010
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Liao, Yen-Shun. “Study the functional region involves in targeting of KChIP1 to membrane.” 2008. Thesis, NSYSU. Accessed January 19, 2021.
http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0715108-124010.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Liao, Yen-Shun. “Study the functional region involves in targeting of KChIP1 to membrane.” 2008. Web. 19 Jan 2021.
Vancouver:
Liao Y. Study the functional region involves in targeting of KChIP1 to membrane. [Internet] [Thesis]. NSYSU; 2008. [cited 2021 Jan 19].
Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0715108-124010.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Liao Y. Study the functional region involves in targeting of KChIP1 to membrane. [Thesis]. NSYSU; 2008. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0715108-124010
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
NSYSU
4.
Kuo, Lai-Hsin.
HDGF Up-regulation Enhances the Invasive Capability and Metastatic Potential of Melanoma Cells.
Degree: Master, Institute of Biomedical Sciences, 2008, NSYSU
URL: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0814108-003244
► Cutaneous malignant melanoma is the fastest increasing malignancy in humans. Hepatoma-derived growth factor (HDGF) is a novel growth factor identified from human hepatoma cell line.…
(more)
▼ Cutaneous malignant melanoma is the fastest increasing malignancy in humans. Hepatoma-derived growth factor (HDGF) is a novel growth factor identified from human hepatoma cell line. HDGF overexpression is correlated with poor prognosis in various types of cancer including melanoma. However, the underlying mechanism of HDGF overexpression during melanoma carcinogenesis remains unclear. In this study, adding exogenous HDGF stimulated the invasion and colonies formation of B16-F10 melanoma cells. Adenovirus vectors encoding HDGF and HDGF-RNAi were generated and characterized to up- and down-regulated HDGF expression in B16-F10 melanoma cells. It was found that HDGF overexpression stimulated the proliferation, invasiveness, anchorage-independent growth of B16-F10 melanoma cells whereas HDGF knockdown exerted opposite effects. In lung-metastasis model, intravenous injection of HDGF-overexpressing melanoma cells resulted in increased metastasis while HDGF-downregulated melanoma cells caused decreased metastasis. Similarly, in primary melanoma model, subcutaneous injection of HDGF-overexpressing melanoma cells enhanced while HDGF-downregulated melanoma cells reduced the tumor burden in mice. Histological analysis revealed increased tumor proliferation and neovascularization with concomitant reduction of apoptosis in HDGF-overexpressing melanoma. Moreover, HDGF-overexpressing melanoma also exhibited enhanced propensity to metastasize from the primary tumors to lymph node and lung. Finally, it was found that HDGF overexpression increased nuclear factor kappa B (NFκB) activities and Akt phosphorylation up and down stream alternation like PI3K, PTEN, IκB and itâs subunit IKKα, IKKβ, IKKγ in melanoma cells. It also found that HDGF overexpression influenced MITF and HIF1α in melanoma after gene delivery. HDGF also altered EMT changes like E,N-cadherin, vimentin, and β,γ-catenin. The present study provides conclusive evidence that HDGF upregulation promotes the growth and metastasis of melanoma by promoting the survival and vascularization. Besides, HDGF knockdown may constitute a novel strategy for melanoma control.
Advisors/Committee Members: Chun%20Hung%22%29&pagesize-30">
Wen-
Chun Hung (chair),
Hurng-Wern Huang (committee member),
Ming-Hong Tai (committee member).
Subjects/Keywords: tumorigenesis; angiogenesis; Melanoma; hepatoma-derived growth factor; HDGF
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APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
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Manager
APA (6th Edition):
Kuo, L. (2008). HDGF Up-regulation Enhances the Invasive Capability and Metastatic Potential of Melanoma Cells. (Thesis). NSYSU. Retrieved from http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0814108-003244
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Kuo, Lai-Hsin. “HDGF Up-regulation Enhances the Invasive Capability and Metastatic Potential of Melanoma Cells.” 2008. Thesis, NSYSU. Accessed January 19, 2021.
http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0814108-003244.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Kuo, Lai-Hsin. “HDGF Up-regulation Enhances the Invasive Capability and Metastatic Potential of Melanoma Cells.” 2008. Web. 19 Jan 2021.
Vancouver:
Kuo L. HDGF Up-regulation Enhances the Invasive Capability and Metastatic Potential of Melanoma Cells. [Internet] [Thesis]. NSYSU; 2008. [cited 2021 Jan 19].
Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0814108-003244.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Kuo L. HDGF Up-regulation Enhances the Invasive Capability and Metastatic Potential of Melanoma Cells. [Thesis]. NSYSU; 2008. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0814108-003244
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
NSYSU
5.
Liu, Yi-Jia.
Study of Kazal motifs of RECK protein on MMP-2 and MMP-9 activity and metastasis of lung adenocarcinoma.
Degree: Master, Institute of Biomedical Sciences, 2009, NSYSU
URL: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0806109-130653
► RECK stands for âreversion-inducing cysteine-rich protein with Kazal motifsâ. This gene was initially discovered by screening a human fibroblast cDNA library for genes giving rise…
(more)
▼ RECK stands for âreversion-inducing cysteine-rich protein with Kazal motifsâ. This gene was initially discovered by screening a human fibroblast cDNA library for genes giving rise to reversion-inducing clones when transfected into v-Ki-ras transformed NIH3T3 cells. The key action of RECK is to inhibit matrix metalloproteinases (MMPs), and it has a significant effect on limiting tumor invasion. Located within the middle part of RECK protein are three serine protease inhibitor-like (SPI) domains (635-654,716-735 and 754-772 amino acids, respectively) which are similar to Kazal motif. Kazal motif is a peptidase inhibitor motif containing disulfide bonds with small alpha and beta folds. The first of these SPI is identical to the Kazal motif (named as K1) and the other two SPIs are highly similar to the Kazal motif (named as K2 & K3). Given RECK is a MMP inhibitor, these SPI-like domains are likely to have a significant role in MMP inhibition.
Our previous data indicated that K23 motifs of RECK protein can inhibit MMP-9 secretion and activity and attenuate metastasis of lung cancer cells. To go a step further, we constructed secretory mammalian expression vectors which could produce K1, K2 and K3 to investigate their effect on MMP activity and cell invasion. We found that K2 also exhibited inhibitory activity on MMP activity and cell invasion. Thus, these finding indicate that the K2 domain of RECK function may be developed as a peptide inhibitor of tumor invasion.
Advisors/Committee Members: Long-sen Chang (chair), Chun%20Hung%22%29&pagesize-30">
Wen-
Chun Hung (committee member),
Hui-Chiu Chang (chair).
Subjects/Keywords: RECK; MMP-9
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APA ·
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MLA ·
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Manager
APA (6th Edition):
Liu, Y. (2009). Study of Kazal motifs of RECK protein on MMP-2 and MMP-9 activity and metastasis of lung adenocarcinoma. (Thesis). NSYSU. Retrieved from http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0806109-130653
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Liu, Yi-Jia. “Study of Kazal motifs of RECK protein on MMP-2 and MMP-9 activity and metastasis of lung adenocarcinoma.” 2009. Thesis, NSYSU. Accessed January 19, 2021.
http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0806109-130653.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Liu, Yi-Jia. “Study of Kazal motifs of RECK protein on MMP-2 and MMP-9 activity and metastasis of lung adenocarcinoma.” 2009. Web. 19 Jan 2021.
Vancouver:
Liu Y. Study of Kazal motifs of RECK protein on MMP-2 and MMP-9 activity and metastasis of lung adenocarcinoma. [Internet] [Thesis]. NSYSU; 2009. [cited 2021 Jan 19].
Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0806109-130653.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Liu Y. Study of Kazal motifs of RECK protein on MMP-2 and MMP-9 activity and metastasis of lung adenocarcinoma. [Thesis]. NSYSU; 2009. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0806109-130653
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
NSYSU
6.
Chiang, Chi-hsiang.
Inhibition of sialylation of beta1 integrin and CXCR4 by a lithocholic acid-based sialyltransferase inhibitor suppresses cancer metastasis.
Degree: Master, Institute of Biomedical Sciences, 2009, NSYSU
URL: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0811109-180108
► Sialyltransferases (STs), which catalyze the sialylation reaction by adding sialic acids to the terminal positions of oligosaccharide of glycoproteins and glycolipids, are over-expressed in cancer…
(more)
▼ Sialyltransferases (STs), which catalyze the sialylation reaction by
adding sialic acids to the terminal positions of oligosaccharide of
glycoproteins and glycolipids, are over-expressed in cancer cells
and associated with cancer metastasis. Until now, ST inhibitors
are not applicable for clinical use because of poor cell
permeability, although showing potent effect in vitro. In this study,
we synthesize a lithocholic acid-based ST inhibitor AL10 and test
its anti-metastatic effect. Overexpression of α-2,3-ST is found in
highly metastatic A549 and CL1-5 lung cancer cells. Confocal
microscopy demonstrates that AL10 is cell permeable and may
attenuate total sialylation on cell surface. AL10 has no cytotoxicity
but inhibits adhesion, migration, actin polymerization and invasion
of A549 and CL1-5 cells in vitro. Inhibition of adhesion and
migration by AL10 is associated with reduced sialylation of beta1
integrin. In addition, activation of the beta1 integrin downstream
signaling molecule focal adhesion kinase is also attenuated. More
importantly, AL10 suppresses lung metastasis in vivo and this
effect may be linked with reduced sialylation of the chemokine
receptor CXCR4 which has been found to play a critical role in
organ-specific metastasis. Serum biochemical assay indicates that
AL10 does not affect liver and kidney functions of experimental
animals. Taken together, we conclude that AL10 is an effective
sialyltransferase inhibitor and exerts anti-metastatic effect in vivo
via suppression of sialylation of beta1 integrin and CXCR4.
Advisors/Committee Members: Hui-Chiu Chang (chair), Chun%20Hung%22%29&pagesize-30">
Wen-
Chun Hung (committee member),
Long-Sen Chang (chair).
Subjects/Keywords: chemokine receptor; sialylation; sialyltransferase; sialic acid
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APA ·
Chicago ·
MLA ·
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CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Chiang, C. (2009). Inhibition of sialylation of beta1 integrin and CXCR4 by a lithocholic acid-based sialyltransferase inhibitor suppresses cancer metastasis. (Thesis). NSYSU. Retrieved from http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0811109-180108
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Chiang, Chi-hsiang. “Inhibition of sialylation of beta1 integrin and CXCR4 by a lithocholic acid-based sialyltransferase inhibitor suppresses cancer metastasis.” 2009. Thesis, NSYSU. Accessed January 19, 2021.
http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0811109-180108.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Chiang, Chi-hsiang. “Inhibition of sialylation of beta1 integrin and CXCR4 by a lithocholic acid-based sialyltransferase inhibitor suppresses cancer metastasis.” 2009. Web. 19 Jan 2021.
Vancouver:
Chiang C. Inhibition of sialylation of beta1 integrin and CXCR4 by a lithocholic acid-based sialyltransferase inhibitor suppresses cancer metastasis. [Internet] [Thesis]. NSYSU; 2009. [cited 2021 Jan 19].
Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0811109-180108.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Chiang C. Inhibition of sialylation of beta1 integrin and CXCR4 by a lithocholic acid-based sialyltransferase inhibitor suppresses cancer metastasis. [Thesis]. NSYSU; 2009. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0811109-180108
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
NSYSU
7.
Chuang, Chun-Wei.
Study of the molecular mechanism by which COX-2 regulates CCR7 expression.
Degree: Master, Institute of Biomedical Sciences, 2010, NSYSU
URL: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0823110-172725
► The metastatic spread of tumor cells is the major lethal aspect of cancer, and lymphatic metastasis is one of the most important routes. Recent studies…
(more)
▼ The metastatic spread of tumor cells is the major lethal aspect of cancer, and lymphatic metastasis is one of the most important routes. Recent studies indicated that cyclooxygenase-2 (COX-2) expression is frequently associated with lymph node metastasis and over-expression of COX-2 can enhance lymphatic invasion of cancer cells. The interaction of chemokines and their cognate receptors also plays a critical role in cancer metastasis. Previous results of our laboratory demonstrated that CCR7 is a downstream target for COX-2 and COX-2 up-regulated CCR7 expression via the EP2 and EP4 receptor. We also found that protein kinase A (PKA) and AKT kinase are involved in COX-2-induced CCR7. In this study, we provided further evidences that COX-2 directly stimulates CCR7 expression via promoter activation. Promoter deletion and mutation assay indicated that COX-2 stimulated CCR7 promoter via the Sp1 binding site located at the -61/-52 bp region upstream of the transcription start site. Increase of Sp1 binding to CCR7 promoter by COX-2 was confirmed by chromatin immunoprecipitation (ChIP) assay. Furthermore, knockdown of Sp1 expression resulted in inhibition of PGE2-induced CCR7, and over-expression of Sp1 potently up-regulated CCR7 in MCF-7 cells. In vitro kinase assay indicated that AKT could directly phosphorylate Sp1 at S42, T679 and S698 sites. And the phosphorylation of Sp1 by AKT led to enhanced protein stability and DNA binding affinity of Sp1. The results of immunohistochemistry indicated that CCR7 expression was significantly associated with Sp1 and phosphor-AKT. Taken together, COX-2 may act via the EP receptor/PKA/AKT/Sp1 signaling pathway to stimulate CCR7 expression in breast cancer cells to promote lymphatic spread.
Advisors/Committee Members: Yow-Ling Shiue (chair), Long-Sen Chang (chair), Chun%20Hung%22%29&pagesize-30">
Wen-
Chun Hung (committee member).
Subjects/Keywords: Sp1; CCR7; AKT; COX-2
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APA (6th Edition):
Chuang, C. (2010). Study of the molecular mechanism by which COX-2 regulates CCR7 expression. (Thesis). NSYSU. Retrieved from http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0823110-172725
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Chuang, Chun-Wei. “Study of the molecular mechanism by which COX-2 regulates CCR7 expression.” 2010. Thesis, NSYSU. Accessed January 19, 2021.
http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0823110-172725.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Chuang, Chun-Wei. “Study of the molecular mechanism by which COX-2 regulates CCR7 expression.” 2010. Web. 19 Jan 2021.
Vancouver:
Chuang C. Study of the molecular mechanism by which COX-2 regulates CCR7 expression. [Internet] [Thesis]. NSYSU; 2010. [cited 2021 Jan 19].
Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0823110-172725.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Chuang C. Study of the molecular mechanism by which COX-2 regulates CCR7 expression. [Thesis]. NSYSU; 2010. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0823110-172725
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
NSYSU
8.
Chen, Chien-wei.
Down-regulation of Jab1 by ER stress in Hep3B hepatocellular carcinoma cell line.
Degree: Master, Institute of Biomedical Sciences, 2009, NSYSU
URL: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0727109-113910
► Endoplasmic reticulum (ER) stress is the condition that unfolded or misfolded proteins accumulated in the ER which leads to the solubility stress. ER can activate…
(more)
▼ Endoplasmic reticulum (ER) stress is the condition that unfolded or misfolded proteins accumulated in the ER which leads to the solubility stress. ER can activate the unfolded protein response (UPR) to restore the ER homeostasis. JAB1 was originally identified as the coactivator of AP-1 transcription factor. JAB1 was then discovered to mediate the cyclin-dependent-kinase inhibitor p27kip1 nuclear exportation and degradation. Previous studies demonstrate that ER stress may affect the regulation of JAB1, but the mechanism is still unknown. In this study, we want to investigate how JAB1 is regulated in ER stress. We applied tunicamycin, a protein N-glycosylation inhibitor, as the ER stress inducer. Western blot and reverse transcription PCR revealed that treatment with tunicamycin for 48 hours in Hep3B induced ER stress and repressed JAB1 protein and mRNA expression. Serial deletion of the JAB1 promoter activity assay revealed that the region from -405 bp to -223 bp may be responsive in the tunicamycin-induced ER stress. Computational prediction suggested that there are several candidate factors may join the regulation of JAB1 in this region. Site-directed mutation of JAB1 promoter assay revealed that the tunicamycin-induced ER stress repressed JAB1 promoter activity through the sites at -342/-338 and -331/-327 in JAB1 promoter. Chromatin immunoprecipitation assay suggested that tunicamycin-induced ER stress repressed the JAB1 promoter activity through increasing the SP1 and DNMT3b binding to the SP1 binding sites at -342/-338 and -331/-327 in JAB1 promoter. Methylation specific PCR showed that the SP1 binding sites at -342/-338 and -331/-327 in JAB1 promoter were methylated in tunicamycin-induced ER stress. Taken together, we demonstrated that tunicamycin-induced ER stress repressed the JAB1 gene expression in Hep3B through increasing the binding of SP1 and DNMT3b to the SP1 binding sites and inducing promoter methylation to repress JAB1 expression.
Advisors/Committee Members: Hui-Chiu Chang (chair), Chun%20Hung%22%29&pagesize-30">
Wen-
Chun Hung (committee member),
Long-sen Chang (chair).
Subjects/Keywords: jab1; er stress
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APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Chen, C. (2009). Down-regulation of Jab1 by ER stress in Hep3B hepatocellular carcinoma cell line. (Thesis). NSYSU. Retrieved from http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0727109-113910
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Chen, Chien-wei. “Down-regulation of Jab1 by ER stress in Hep3B hepatocellular carcinoma cell line.” 2009. Thesis, NSYSU. Accessed January 19, 2021.
http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0727109-113910.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Chen, Chien-wei. “Down-regulation of Jab1 by ER stress in Hep3B hepatocellular carcinoma cell line.” 2009. Web. 19 Jan 2021.
Vancouver:
Chen C. Down-regulation of Jab1 by ER stress in Hep3B hepatocellular carcinoma cell line. [Internet] [Thesis]. NSYSU; 2009. [cited 2021 Jan 19].
Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0727109-113910.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Chen C. Down-regulation of Jab1 by ER stress in Hep3B hepatocellular carcinoma cell line. [Thesis]. NSYSU; 2009. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0727109-113910
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
NSYSU
9.
Su, Huei-Ting.
The Stem Cell Marker Nestin is Critical for TGF beta1- Mediated Tumor Progression in Pancreatic Cancer.
Degree: Master, Institute of Biomedical Sciences, 2012, NSYSU
URL: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0625112-152043
► Stem cell marker Nestin is an intermediate filament protein that plays an important role in cell integrity, migration and differentiation. Nestin expression occurs in approximately…
(more)
▼ Stem cell marker Nestin is an intermediate filament protein that plays an important role in cell integrity, migration and differentiation. Nestin expression occurs in approximately one-third of pancreatic ductal adenocarcinoma (PDAC) cases, and its expression positively correlates with tumor stage and peripancreatic invasion. Little is known of the mechanisms by which Nestin influences PDAC progression. We showed that Nestin overexpression in PDAC cells increased cell motility and drove phenotypic changes associated with the epithelial-mesenchymal transition in vitro, conversely, knockdown of endogenous Nestin expression reduced the migration rate and cells reverted to a more epithelial phenotype. In vivo mice studies showed that knockdown of Nestin significantly reduced tumor incidence and volume in xenografts. Expression of the Nestin protein was associated with Smad4 status in PDAC cells, hence Nestin expression might be regulated by the TGF-b1/SMAD4 pathway in PDAC. We examined Nestin expression after TGF-b1 treatment in human pancreatic cancer PANC-1, and PANC-1 shSmad4 cells. The TGF-b/SMAD pathway induced Nestin protein expression in PDAC cells through Smad4 in a dependent manner. Moreover, increased Nestin expression caused a positive feedback loop in the TGFb/SMAD signaling system.
Finally, we demonstrated that 2 anti-microtubule inhibitors, Cytochalasin D (CD) and Withaferin A (WFA), exhibited anti-Nestin activity; these inhibitors might be potential anti-metastatic drugs. Our findings uncovered a novel role of Nestin in regulating TGF-b1-induced EMT. Anti-Nestin therapeutics are under development as a potential treatment for PDAC metastasis.
Advisors/Committee Members: Chun%20Hung%22%29&pagesize-30">
Wen-
Chun Hung (chair),
hung%20Cheng%22%29&pagesize-30">Kuang-hung Cheng (committee member),
Long-Sen Chang (chair),
Hurng-Wern Huang (chair).
Subjects/Keywords: EMT; Intermediate filament proteins; Nestin; PDAC
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APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Su, H. (2012). The Stem Cell Marker Nestin is Critical for TGF beta1- Mediated Tumor Progression in Pancreatic Cancer. (Thesis). NSYSU. Retrieved from http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0625112-152043
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Su, Huei-Ting. “The Stem Cell Marker Nestin is Critical for TGF beta1- Mediated Tumor Progression in Pancreatic Cancer.” 2012. Thesis, NSYSU. Accessed January 19, 2021.
http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0625112-152043.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Su, Huei-Ting. “The Stem Cell Marker Nestin is Critical for TGF beta1- Mediated Tumor Progression in Pancreatic Cancer.” 2012. Web. 19 Jan 2021.
Vancouver:
Su H. The Stem Cell Marker Nestin is Critical for TGF beta1- Mediated Tumor Progression in Pancreatic Cancer. [Internet] [Thesis]. NSYSU; 2012. [cited 2021 Jan 19].
Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0625112-152043.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Su H. The Stem Cell Marker Nestin is Critical for TGF beta1- Mediated Tumor Progression in Pancreatic Cancer. [Thesis]. NSYSU; 2012. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0625112-152043
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
NSYSU
10.
Lin, Hsin-Ying.
STAT3-upregulated miR-92a in the control RECK expression in lung cancer cells.
Degree: Master, Institute of Biomedical Sciences, 2012, NSYSU
URL: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0706112-173625
► Lung cancer is the common cause of cancer death. STAT3 (signal transducer and activator of transcription 3) has been reported to be an oncogenic transcription…
(more)
▼ Lung cancer is the common cause of cancer death. STAT3 (signal transducer and activator of transcription 3) has been reported to be an oncogenic transcription factor and high expression of STAT3 is associated with lung cancer progression. RECK (reversion-inducing cysteine-rich protein with Kazal motifs) is a tumor suppressor gene and a membrane-anchored glycoprotein that reduces the matrix metalloproteinases (MMPs)-induced destruction of extra-cellular matrix (ECM) and tumor metastasis. RECK also inhibits tumor angiogenesis. We have previously elucidated the transcriptional regulation of RECK gene. Recently, microRNAs (miRs) are shown to be key players in gene regulation and cancer progression. In this study, we try to elucidate whether ovexpression of STAT3 can affect microRNA expression to regulate RECK via post-transcriptional modulation. miR-17-92a cluster is a well-known oncomir which is highly expressed in lung cancer tissue. We find that miR-92a, a member of miR-17-92a cluster can target RECK 3âUTR. In addition, our data suggest that STAT3 regulates the expression of miR-92a and inhibition of STAT3 can decrease miR-92a expression. Furthermore, overexpression of miR-92a can decrease RECK protein level. While knockdown of miR-92a expression in STAT3-overexpressing cell lines can restore RECK protein level, and reduce invasion and migration. Results of this study suggest that STAT3 up-regulates miR-92a to inhibit RECK expression and promote lung cancer metastasis.
Advisors/Committee Members: Po-Lin Kuo (chair), Hung%20Cheng%22%29&pagesize-30">Kuang-
Hung Cheng (chair),
Chun%20Hung%22%29&pagesize-30">Wen-Chun Hung (committee member).
Subjects/Keywords: RECK; miR-92a; STAT3
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Lin, H. (2012). STAT3-upregulated miR-92a in the control RECK expression in lung cancer cells. (Thesis). NSYSU. Retrieved from http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0706112-173625
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Lin, Hsin-Ying. “STAT3-upregulated miR-92a in the control RECK expression in lung cancer cells.” 2012. Thesis, NSYSU. Accessed January 19, 2021.
http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0706112-173625.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Lin, Hsin-Ying. “STAT3-upregulated miR-92a in the control RECK expression in lung cancer cells.” 2012. Web. 19 Jan 2021.
Vancouver:
Lin H. STAT3-upregulated miR-92a in the control RECK expression in lung cancer cells. [Internet] [Thesis]. NSYSU; 2012. [cited 2021 Jan 19].
Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0706112-173625.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Lin H. STAT3-upregulated miR-92a in the control RECK expression in lung cancer cells. [Thesis]. NSYSU; 2012. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0706112-173625
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
NSYSU
11.
Ye, Min-Yi.
Anti-cancer mechanism of a novel tyrosine kinase inhibitor on human lung cancer cells.
Degree: Master, Institute of Biomedical Sciences, 2012, NSYSU
URL: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0706112-184416
► Tyrosine kinases regulate fundamental signal pathways in cells including cell proliferation, motility, and differentiation. The kinase activity is tightly controlled in normal cells but is…
(more)
▼ Tyrosine kinases regulate fundamental signal pathways in cells including cell proliferation, motility, and differentiation. The kinase activity is tightly controlled in normal cells but is usually excessive activated in cancers. Several tyrosine kinase inhibitors are used in cancer therapies nowadays. Our novel tyrosine kinase inhibitor, 1J-309, is a multiple kinase inhibitor that targets several receptors including vascular endothelial growth factor receptors (VEGFRs). We find 1J-309 dramatically reduces cell proliferation of VEGFR3+/VEGF-C+ A549 human lung cancer cells by decreasing the expression of CDK1 and cyclin B1 following growth arrest at G2/M phase. After long term drug treatment, 1J-309 causes cell death. Moreover, 1J-309 represses CDK1 expression at early stage but it does not change CDK1 RNA expression and protein stability. Additionally, 1J-309 significantly decreases the migration ability of A549 cells. 1J-309 also reduces gelatin-related invasion potency. The AKT and p38 MAPK activity are significantly repressed by 1J-309 and it dramatically drives the expression of tumor suppressor, p53, at low-dose treatment. Our results demonstrate that 1J-309 significantly attenuates cell proliferation by inducing G2/M growth arrest, reduces the invasion and migration potency, and promotes a dramatic increase of p53 in A549 cells.
Advisors/Committee Members: Hung%20Cheng%22%29&pagesize-30">Kuang-
Hung Cheng (chair),
Chun%20Hung%22%29&pagesize-30">Wen-Chun Hung (committee member),
Po-Lin Kuo (chair).
Subjects/Keywords: p53; migration; CDK1; lung cancer; tyrosine kinase inhibitor
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APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Ye, M. (2012). Anti-cancer mechanism of a novel tyrosine kinase inhibitor on human lung cancer cells. (Thesis). NSYSU. Retrieved from http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0706112-184416
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Ye, Min-Yi. “Anti-cancer mechanism of a novel tyrosine kinase inhibitor on human lung cancer cells.” 2012. Thesis, NSYSU. Accessed January 19, 2021.
http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0706112-184416.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Ye, Min-Yi. “Anti-cancer mechanism of a novel tyrosine kinase inhibitor on human lung cancer cells.” 2012. Web. 19 Jan 2021.
Vancouver:
Ye M. Anti-cancer mechanism of a novel tyrosine kinase inhibitor on human lung cancer cells. [Internet] [Thesis]. NSYSU; 2012. [cited 2021 Jan 19].
Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0706112-184416.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Ye M. Anti-cancer mechanism of a novel tyrosine kinase inhibitor on human lung cancer cells. [Thesis]. NSYSU; 2012. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0706112-184416
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
NSYSU
12.
Su, Mei-lin.
Sialylation of CCR7 is critical for CCL19-stimulated proliferation, invasion and anti-anoikis in breast cancer cells.
Degree: Master, Institute of Biomedical Sciences, 2012, NSYSU
URL: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0716112-124147
► Sialylation is catalyzed by sialyltransferases (STs) that adding sialic acids to the terminal positions of oligosaccharide of glycoproteins and glycolipids. This process is frequently enhanced…
(more)
▼ Sialylation is catalyzed by sialyltransferases (STs) that adding sialic acids to the
terminal positions of oligosaccharide of glycoproteins and glycolipids. This process is
frequently enhanced in cancer and is associated with increased cancer metastasis. Recent
studies demonstrated that over-expression of ST3Gal-I promotes mammary
tumorigenesis. In our experiments, we also find overexpression of α-2,3-ST in breast
cancer cells. We previously synthesized a lithocholic acid-based ST inhibitor AL10 and
demonstrated its anti-metastatic effect in vitro and in vivo. Our results showed that
AL10 is an effective sialyltransferase inhibitor and exerts anti-metastatic effect in vivo
via suppression of sialylation of beta1 integrin and CXCR4. Breast cancer cells
expressing high level of chemokine receptors CXCR4 and CCR7 are prone to exhibit
lymphatic metastasis because their cognate ligands CCL19, CCL21 and SDF-1 are
continuously expressed by lymphatic endothelial cells. In this study, we demonstrate
that AL10 can inhibit invasion, proliferation and induce anoikis of
α-2,3-ST-overexpressing MDA-MB231 human breast cancer cells. Our results indicate
that inhibition of CCL19-induced invasion and CCL19-reduced anoikis by AL10 are
associated with reduced sialylation of CCR7 and attenuated activation of the
downstream signaling mediator ERK and p38. In addition, AL10 can inhibit
proliferation by reducing activation of AKT via CCR7 sialylation independent pathway
and p-38 via CCR7 sialylation dependent pathway which results in ubiquitin-dependent
cyclin D1 degradation. Taken together, we conclude that sialylation of CCR7 is critical
for CCL19-stimulated proliferation, invasion and anti-anoikis in breast cancer cells.
Advisors/Committee Members: Po-lin Kuo (chair), Chun%20Hung%22%29&pagesize-30">
Wen-
Chun Hung (committee member),
hung%20Cheng%22%29&pagesize-30">Kuang-hung Cheng (chair).
Subjects/Keywords: sialylation; CCR7; metastasis; AL10; breast cancer
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APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Su, M. (2012). Sialylation of CCR7 is critical for CCL19-stimulated proliferation, invasion and anti-anoikis in breast cancer cells. (Thesis). NSYSU. Retrieved from http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0716112-124147
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Su, Mei-lin. “Sialylation of CCR7 is critical for CCL19-stimulated proliferation, invasion and anti-anoikis in breast cancer cells.” 2012. Thesis, NSYSU. Accessed January 19, 2021.
http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0716112-124147.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Su, Mei-lin. “Sialylation of CCR7 is critical for CCL19-stimulated proliferation, invasion and anti-anoikis in breast cancer cells.” 2012. Web. 19 Jan 2021.
Vancouver:
Su M. Sialylation of CCR7 is critical for CCL19-stimulated proliferation, invasion and anti-anoikis in breast cancer cells. [Internet] [Thesis]. NSYSU; 2012. [cited 2021 Jan 19].
Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0716112-124147.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Su M. Sialylation of CCR7 is critical for CCL19-stimulated proliferation, invasion and anti-anoikis in breast cancer cells. [Thesis]. NSYSU; 2012. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0716112-124147
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
NSYSU
13.
Weng, Ching-Chieh.
The Role of CD133 to Bind to EGFR and Modulate Its Activation in Pancreatic Cancer.
Degree: Master, Institute of Biomedical Sciences, 2012, NSYSU
URL: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0823112-145009
► Most of tumor consists of a heterogeneous population of tumor cells among a tumor initiating and chemo or radiation resistant subpopulation, called cancer stem cells…
(more)
▼ Most of tumor consists of a heterogeneous population of tumor cells among a tumor initiating and chemo or radiation resistant subpopulation, called cancer stem cells (CSCs), which have become increasingly important new anticancer targets. CD133 has been recently identified as a prominent marker for CSCs in pancreatic and other tumors; however, the signaling cascade of this cancer stem cell marker has not been fully explored. This study shows increased cell proliferation, colony formation, adhesion, and migration following CD133 overexpression in pancreatic ductal adenocarcinoma (PDAC) cells. Signaling studies have indicated that CD133 overexpression increases the epidermal growth factor receptor (EGFR) activation and phosphorylation of PI3K/Akt and MAPK/ ERK pathways. An in vivo xenograft study confirmed that overexpression of CD133 has higher tumorgentic ability than control mice. Molecular studies have found that CD133 physically associates with EGFR and promotes EGFR protein level and its phosphorlyation, which might be critical for PDAC tumor progression and chemoresistance. The data also showed that CD133 overexpression suppresses the EGF mRNA expression, which may imply that CD133 induces EGFR activation through an EGF ligand-independent process. The findings here point to an important mechanism of action for CD133 in PDAC. The EGFR inhibitor has potent anti-CD133 activity, and the current results have important implications for developing targeting CD133 activity as a novel cancer therapy strategy and the inhibitor approach presented here identifies the inhibition of CD133 activity by the EGFR inhibitor and sheds light on developing a new cancer therapeutic that functions by targeting CD133 activity in human cancer.
Advisors/Committee Members: Wen%20Huang%22%29&pagesize-30">
Hung-
Wen Huang (chair),
Long-Sen Chang (chair),
Hung%20Cheng%22%29&pagesize-30">Kuang -Hung Cheng (committee member),
Chun%20Hung%22%29&pagesize-30">Wen-Chun Hung (chair).
Subjects/Keywords: Cancer stem cells; CD133; Epidermal Growth Factor Receptor; MAPK/ ERK pathways
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APA ·
Chicago ·
MLA ·
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CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Weng, C. (2012). The Role of CD133 to Bind to EGFR and Modulate Its Activation in Pancreatic Cancer. (Thesis). NSYSU. Retrieved from http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0823112-145009
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Weng, Ching-Chieh. “The Role of CD133 to Bind to EGFR and Modulate Its Activation in Pancreatic Cancer.” 2012. Thesis, NSYSU. Accessed January 19, 2021.
http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0823112-145009.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Weng, Ching-Chieh. “The Role of CD133 to Bind to EGFR and Modulate Its Activation in Pancreatic Cancer.” 2012. Web. 19 Jan 2021.
Vancouver:
Weng C. The Role of CD133 to Bind to EGFR and Modulate Its Activation in Pancreatic Cancer. [Internet] [Thesis]. NSYSU; 2012. [cited 2021 Jan 19].
Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0823112-145009.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Weng C. The Role of CD133 to Bind to EGFR and Modulate Its Activation in Pancreatic Cancer. [Thesis]. NSYSU; 2012. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0823112-145009
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
NSYSU
14.
Wu, Nein-chi.
Single Nucleotide Polymorphism Analysis of the Metastasis Supressor RECK Gene Promoter and Itâs Clinical Significance.
Degree: Master, Institute of Biomedical Sciences, 2011, NSYSU
URL: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0809111-202826
► Reversion-inducing cysteine-rich with Kazal motif (RECK) is a cell surface anchoring protein, which known for the ability to inhibit matrix metalloproteinases (MMPs) and participate in…
(more)
▼ Reversion-inducing cysteine-rich with Kazal motif (RECK) is a cell surface anchoring protein, which known for the ability to inhibit matrix metalloproteinases (MMPs) and participate in angiogenesis regulation. The inhibition of membrane type-1 matrix metalloproteinase (MT1-MMP), MMP-2, MMP-7 and, MMP-9 by RECK has been demonstrated.
Our previous studies show that RECK expression is suppressed by Ras and Her-2/neu oncogene. In addition, oncogenic Ras activates downstream ERK signaling pathway to increase Sp1/HDAC promoter binding affinity which results in reduction of RECK gene transcription and increase of tumor progression and metastasis.
From the clinical investigation, RECK expression is down-regulated in a number of cancer types. In breast cancer, RECK expression is associated with the prognosis of the patients. Recently, single nucleotide polymorphisms (SNPs) of RECK promoter have been suggested to be linked with survival rate and prognosis of breast cancer patients. Whether SNP of the RECK promoter has any effect on RECK expression and its clinical significance is still unclear. .
In this study, we investigate -402 SNP at RECK promoter and find this SNP directly affects RECK expression through progesterone receptor binding. Additionally, we also address the -402 SNP in the sample collected from patients and analyze its association with clinicopathological parameters to clarify its clinical significance. Our results suggest that RECK SNP may be an valuable prognosis factor for breast cancer.
Advisors/Committee Members: Hung-shu Chang (chair), chun%20Hung%22%29&pagesize-30">
Wen-
chun Hung (committee member),
Kwan-hon Cheng (chair).
Subjects/Keywords: RECK promoter; Reversion-inducing cysteine-rich with Kazal motif; RECK; RECK SNP; SNP; single nucleotide polymorphism
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APA (6th Edition):
Wu, N. (2011). Single Nucleotide Polymorphism Analysis of the Metastasis Supressor RECK Gene Promoter and Itâs Clinical Significance. (Thesis). NSYSU. Retrieved from http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0809111-202826
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Wu, Nein-chi. “Single Nucleotide Polymorphism Analysis of the Metastasis Supressor RECK Gene Promoter and Itâs Clinical Significance.” 2011. Thesis, NSYSU. Accessed January 19, 2021.
http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0809111-202826.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Wu, Nein-chi. “Single Nucleotide Polymorphism Analysis of the Metastasis Supressor RECK Gene Promoter and Itâs Clinical Significance.” 2011. Web. 19 Jan 2021.
Vancouver:
Wu N. Single Nucleotide Polymorphism Analysis of the Metastasis Supressor RECK Gene Promoter and Itâs Clinical Significance. [Internet] [Thesis]. NSYSU; 2011. [cited 2021 Jan 19].
Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0809111-202826.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Wu N. Single Nucleotide Polymorphism Analysis of the Metastasis Supressor RECK Gene Promoter and Itâs Clinical Significance. [Thesis]. NSYSU; 2011. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0809111-202826
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
NSYSU
15.
Chen, Ku-chung.
Cytotoxic mechanisms of Taiwan cobra phospholipase A2.
Degree: PhD, Institute of Biomedical Sciences, 2009, NSYSU
URL: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0903109-184305
► The enzyme phospholipase A2 (PLA2) specifically hydrolyzes the 2-acyl ester bond of 1,2-diacyl-3-sn-phosphoglycerides releasing fatty acids and lysophospholipids in the presence of Ca2+. Both products…
(more)
▼ The enzyme phospholipase A2 (PLA2) specifically hydrolyzes the 2-acyl ester bond of 1,2-diacyl-3-sn-phosphoglycerides releasing fatty acids and lysophospholipids in the presence of Ca2+. Both products represent precursors for signaling molecules that can exert a multitude of biological functions including phospholipid metabolism, exocytosis and inflammation. Consequently, PLA2 not only plays a role in regulating physiological processes, but also exhibits pharmacological effects in inflammatory diseases. Nevertheless, the signaling pathway leading to cell death still remains elusive. In the present study, the cytotoxicity of Naja naja atra PLA2 toward human neuroblastoma SK-N-SH cells and leukemia K562 cells were respectively evaluated to explore the signaling pathway of PLA2-induced cell death. Upon exposure to PLA2, p38 mitogen-activated protein kinase (p38 MAPK) or c-Jun N-terminal kinase (JNK) activation, extracellularsignal-regulated protein kinase (ERK) inactivation, reactive oxygen species (ROS) generation, increase in intracellular Ca2+ concentration, the loss of mitochondrial membrane potential (ÎΨm), cytochrome c release and upregulation of Fas/FasL were found in SK-N-SH or K562 cells. N-Acetylcysteine (ROS scavenger), BAPTA-AM (Ca2+ chelator), SB202190 (p38 MAPK inhibitor) or SP600125 (JNK inhibitor) abrogated p38 MAPK or JNK activation and rescued cell viability, ÎΨm, cytochrome c release and suppressed Fas/FasL upregulation of PLA2-treated cells, but restored phosphorylation of ERK. Activated ERK was found to attenuate p38 MAPK-mediated upregulation of Fas/FasL. Besides, sustained JNK activation was also observed in SB202190/PLA2-treated K562 cells after exterminating p38 MAPK activation, but also retained the cytotoxicity of PLA2. Knockdown of p38 MAPK or JNK1 by siRNA proved that PLA2 induced Fas/FasL upregulation through p38 MAPK/ATF-2 or JNK1/c-Jun pathways in K562 cells. Furthermore, deprivation of catalytic activity could not diminish PLA2-induced cell death and Fas/FasL upregulation.
The cytotoxicity of arachidonic acid (AA) and lysophosphatidylcholine (LPC) was not related to the expression of Fas/FasL. The results showed that the cytotoxicity of AA is mediated through mitochondria-dependent death pathway, eliciting by AA-induced ROS generation and Ca2+-evoked activation of p38 MAPK and JNK. Besides, ERK activation abrogated by U0126 improved the ability of AA-mediated Fas/FasL upregulation in K562 cells. Taken together, our results indicate that PLA2-induced cell death is through Ca2+- and ROS evoked p38 MAPK or JNK activation. Upregulation of Fas/FasL partially involves in cytotoxicity of PLA2.
Advisors/Committee Members: Chun-chang Chang (chair), Chung-yee Yuo (chair), chun%20Hung%22%29&pagesize-30">
Wen-
chun Hung (chair),
Long-sen Chang (committee member),
Shinne-ren Lin (chair).
Subjects/Keywords: arachidonic acid; PLA2; phospholipase A2; FasL; Fas; JNK; ROS; Ca; p38 MAPK; SK-N-SH; lysophosphatidylcholine; K562
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APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
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Manager
APA (6th Edition):
Chen, K. (2009). Cytotoxic mechanisms of Taiwan cobra phospholipase A2. (Doctoral Dissertation). NSYSU. Retrieved from http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0903109-184305
Chicago Manual of Style (16th Edition):
Chen, Ku-chung. “Cytotoxic mechanisms of Taiwan cobra phospholipase A2.” 2009. Doctoral Dissertation, NSYSU. Accessed January 19, 2021.
http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0903109-184305.
MLA Handbook (7th Edition):
Chen, Ku-chung. “Cytotoxic mechanisms of Taiwan cobra phospholipase A2.” 2009. Web. 19 Jan 2021.
Vancouver:
Chen K. Cytotoxic mechanisms of Taiwan cobra phospholipase A2. [Internet] [Doctoral dissertation]. NSYSU; 2009. [cited 2021 Jan 19].
Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0903109-184305.
Council of Science Editors:
Chen K. Cytotoxic mechanisms of Taiwan cobra phospholipase A2. [Doctoral Dissertation]. NSYSU; 2009. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0903109-184305
NSYSU
16.
Chen, Jing-yi.
Regulation of Skp2 by Bcr-ABL oncogene in chronic meyloid leukemia cells and its therapeutic significance.
Degree: PhD, Institute of Biomedical Sciences, 2010, NSYSU
URL: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0802110-181153
► Part I BCR-ABL fusion oncogene results fromt(9;22)(q34;q11) translocation of chromosome is the most common genetic abnormality found in chronic myeloid leukemia (CML) cells . The…
(more)
▼ Part I
BCR-ABL fusion oncogene results fromt(9;22)(q34;q11) translocation of chromosome is the most common genetic abnormality found in chronic myeloid leukemia (CML) cells . The encoded protein of this fusion gene exhibits constitutively active tyrosinekinase activity which is required for the pathogenesis of CML. We addressed how BCR-ABL oncoprotein increased Skp2 expression. Treatment of Imatinib or LY294002 reduced Skp2mRNA in BCR-ABL-positive K562 cells. Knockdown of AKT by small hairpin RNAalso reduced Skp2 expression. We found that BCR-ABL up-regulated Skp2 via Sp1 because (1) the Sp1 site located at the −386/−380 promoter region was important for BCR-ABL-induced Skp2 promoter activity, (2) chromatin immunoprecipitation assay demonstrated that Imatinib inhibited the recruitment of p300 to the Sp1 site of Skp2 promoter and (3) knockdown of Sp1 reduced Skp2 expression in K562 cells. These results suggest that BCR-ABL controls Skp2 gene transcription via the PI3K/AKT/Sp1 pathway. In addition to transcriptional regulation of Skp2, Bcr-Abl also modulates Skp2 protein stability in these cells. Treatment of Bcr-Abl kinase inhibitor imatinib led to G1 growth arrest accompanied with reduced Skp2 expression. Interestingly, reduction of Skp2 protein occurred prior to down-regulation of Skp2 mRNA suggesting a post-translational control. The half-life of Skp2 protein was significantly attenuated in imatinib-treated cells. Knockdown of Bcr-Abl similarly caused Skp2 protein instability. The decrease of Skp2 was induced by increased protein degradation through the ubiquitin/ proteasome pathway. Our results demonstrated that imatinib treatment or Bcr-Abl knockdown reduced Emi1, an endogenous inhibitor of the E3 ligase APC/Cdh1 which mediated the degradation of Skp2 protein. We found that Emi1 stability was regulated by phosphorylation and mutation of tyrosine 142 significantly reduced the stability. Lines of evidence suggested Bcr-Abl-induced Emi1 phosphorylation was mediated by Src kinase. (1) Src inhibitor SU6656 inhibited Emi1 tyrosine phosphorylation in Bcr-Abl-positive K562 cells. (2) Transfection of v-Src rescued the reduction of Emi1 by imatinib. (3) Mutation of tyrosine 142 to phenylalanine (Y142F) abolished the phosphorylation of Emi1 by recombinant Src kinase. In addition, ectopic expression of wild type but not Y142F mutant Emi1 could counteract imatinib-caused G1 growth arrest. Collectively, our results suggest that Bcr-Abl fusion oncogene increases Emi1 phosphorylation and stability to prevent Skp2 protein degradation via APC/Cdh1-induced ubiquitination and to enhance proliferation of CML cells.
Part II
Although imatinib therapy of chronic myelogenous leukemia is effective, the resistance to imatinib challenges the treatment of this disease. Therefore, search of novel drugs to overcome imatinib resistance is a critical issue in clinic. Withaferin A (WA), an extract of Withania somniferia, exhibits anti-cancer activity on a number of solid tumors. In this study, we investigate the effect of WA on imatinib-sensitive…
Advisors/Committee Members: Yow-Ling Shiue (chair), Yeou-Lih Huang (chair), Long-sen Chang (chair), Shinne-Ren Lin (chair), Chun%20Hung%22%29&pagesize-30">
Wen-
Chun Hung (committee member).
Subjects/Keywords: miR-92a; SAHA; withaferin A; Skp2; CML
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APA ·
Chicago ·
MLA ·
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CSE |
Export
to Zotero / EndNote / Reference
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APA (6th Edition):
Chen, J. (2010). Regulation of Skp2 by Bcr-ABL oncogene in chronic meyloid leukemia cells and its therapeutic significance. (Doctoral Dissertation). NSYSU. Retrieved from http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0802110-181153
Chicago Manual of Style (16th Edition):
Chen, Jing-yi. “Regulation of Skp2 by Bcr-ABL oncogene in chronic meyloid leukemia cells and its therapeutic significance.” 2010. Doctoral Dissertation, NSYSU. Accessed January 19, 2021.
http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0802110-181153.
MLA Handbook (7th Edition):
Chen, Jing-yi. “Regulation of Skp2 by Bcr-ABL oncogene in chronic meyloid leukemia cells and its therapeutic significance.” 2010. Web. 19 Jan 2021.
Vancouver:
Chen J. Regulation of Skp2 by Bcr-ABL oncogene in chronic meyloid leukemia cells and its therapeutic significance. [Internet] [Doctoral dissertation]. NSYSU; 2010. [cited 2021 Jan 19].
Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0802110-181153.
Council of Science Editors:
Chen J. Regulation of Skp2 by Bcr-ABL oncogene in chronic meyloid leukemia cells and its therapeutic significance. [Doctoral Dissertation]. NSYSU; 2010. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0802110-181153
NSYSU
17.
Wang, Chi-Hung.
Effects and mechanisms of novel indole compound on the regulation of breast cancer cell growth, invasion and the reversion of epithelial-to-mesenchymal transition.
Degree: PhD, Institute of Biomedical Sciences, 2013, NSYSU
URL: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0712113-113112
► Breast cancer is the leading cause of death among Taiwanese women as well as women all over the world. Epidemiological and dietary studies have shown…
(more)
▼ Breast cancer is the leading cause of death among Taiwanese women as well as women all over the world. Epidemiological and dietary studies have shown that high dietary intake of cruciferous vegetables protect against carcinogenesis. The dietary compound, indole-3-carbinol (I3C), is an autolysis product of glucosinolate, glucobrassicin, which is found in Brassica vegetables such as cabbage, broccoli and brussels sprouts. Indole-3-carbinol and its metabolite 3,3â-diindolylmethane target multiple aspects of cancer cell-cycle regulation and survival including Akt-NFκB signaling, caspase activation, cycle-dependent kinase activities, estrogen receptor signaling, endoplasmic reticulum stress and BRCA gene expression. The development of new and efficient synthetic methods to prepare indole derivatives continues to receive a lot attention in organic synthesis because of their biological activities. Various indole moieties occur in many pharmacologically and biologically active compounds. For instance, the simplest indole derivative such as indole-3-carbinol is a potential inhibitor of the growth of breast cancer and can induce the arrest of the cell cycle in G1 phase. 3, 3â-Diindoylmethane that derived from indole-3-carbinol by acid treatment, is also reported to possess the same activity. Therefore, several research groups are devoted their research towards the synthesis of various indole derivatives.
In the part I, we examined a series of tetraindole related derivatives to explore their cellular cytotoxicity for further development of new chemotherapeutic agents. First, the cytotoxicity was evaluated by MTT assay. The results indicated that a tetraindole derivative named SK228 has the best IC50 value at about 0.45 μM and 0.88 μM in MDA-MB-231 and MCF7 cells respectively. Second, the cell cycle was arrested in G2/M phase by SK228 treatment. Third, the SK228 induces the up-regulation of apoptosis-related proteins, such as bak, activated caspase-3, and cleaved PARP, and the down-regulation of bcl-2. Finally, the degradation of genomic DNA was also induced by SK228 treatment. Taken together; our results suggested the tetraindole derivative, SK228, is a potent chemotherapeutic agent.
In the part II, as I3C can induce the expression of E-cadherin and repress the cancer cells motility in vivo, we hypothesized that SK228 can induce the reversion of epithelial-mesenchymal transition (EMT) via the similar signaling pathway. First, we found that the cell-cell adhesion glycoprotein, E-cadherin, was up-regulated in both RNA and protein levels after SK228 treatment. Second, the in vitro migration and invasion activities of breast cancer cells were repressed by SK228. Moreover, the cell morphology was changed from fibroblastoid to epithelial cobblestone-like appearance after incubated with SK228. Several EMT-inducing transcription factors and E-cadherin transcriptional repressors such as Twist1, ZEB1 (δEF1), ZEB2 (SIP1) and Slug (Snail2) were also down-regulated by SK228. Moreover, we also found SK228 can up-regulate the expression…
Advisors/Committee Members: Chun%20Hung%22%29&pagesize-30">
Wen-
Chun Hung (committee member),
Han-Chung Wu (chair),
Yeou-Lih Huang (chair),
Long-Sen Chang (chair),
Wen-Shan Li (chair).
Subjects/Keywords: epithelial-mesenchymal transition (EMT); miRNA-200; Histone deacetylase (HDAC); E-cadherin; ZEB1; apoptosis; 3,3â-diindolylmethane; Indole-3-carbinol (I3C)
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APA ·
Chicago ·
MLA ·
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Export
to Zotero / EndNote / Reference
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APA (6th Edition):
Wang, C. (2013). Effects and mechanisms of novel indole compound on the regulation of breast cancer cell growth, invasion and the reversion of epithelial-to-mesenchymal transition. (Doctoral Dissertation). NSYSU. Retrieved from http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0712113-113112
Chicago Manual of Style (16th Edition):
Wang, Chi-Hung. “Effects and mechanisms of novel indole compound on the regulation of breast cancer cell growth, invasion and the reversion of epithelial-to-mesenchymal transition.” 2013. Doctoral Dissertation, NSYSU. Accessed January 19, 2021.
http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0712113-113112.
MLA Handbook (7th Edition):
Wang, Chi-Hung. “Effects and mechanisms of novel indole compound on the regulation of breast cancer cell growth, invasion and the reversion of epithelial-to-mesenchymal transition.” 2013. Web. 19 Jan 2021.
Vancouver:
Wang C. Effects and mechanisms of novel indole compound on the regulation of breast cancer cell growth, invasion and the reversion of epithelial-to-mesenchymal transition. [Internet] [Doctoral dissertation]. NSYSU; 2013. [cited 2021 Jan 19].
Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0712113-113112.
Council of Science Editors:
Wang C. Effects and mechanisms of novel indole compound on the regulation of breast cancer cell growth, invasion and the reversion of epithelial-to-mesenchymal transition. [Doctoral Dissertation]. NSYSU; 2013. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0712113-113112
NSYSU
18.
Chu, Tian-huei.
Therapeutic Efficacy and Mechanism of Celecoxib for Hepatocellular Carcinoma.
Degree: PhD, Institute of Biomedical Sciences, 2014, NSYSU
URL: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0809114-182128
► Hepatocellular carcinoma (HCC) is the one of most common malignancies in Taiwan. Current HCC therapies include surgery, chemotherapy, radiofrequency ablation and target therapy. However, the…
(more)
▼ Hepatocellular carcinoma (HCC) is the one of most common malignancies in Taiwan. Current HCC therapies include surgery, chemotherapy, radiofrequency ablation and target therapy. However, the overall prognosis for HCC remains poor. The aim of study is to evaluate the therapeutic efficacy and mechanism of non-steroidal anti-inflammatory drug (NSAID) celecoxib in HCC. Celecoxib is a cyclooxygenase 2 (COX-2) inhibitor. Many reports indicate celecoxib shown chemopreventive effect in many malignancies, especially in colon cancer. But the effect and anti-cancer mechanism of celecoxib in liver cancer is unclear. The present study has further demonstrated the therapeutic efficacy of celecoxib in rat orthotopic HCC model. The mechanism is celecoxib inhibited cancer stem cells expansion and function through up-regulating tumor suppressor gene PTEN to regulate Akt pathway and reducing tumor microenvironmental prostaglandin E2 (PGE2). Moreover, PGE2 induced the expansion of hCSCs mediated EP4 receptor activation.
Sorafenib is the only target therapeutic drug for HCC treatment. However, the cost of Sorafenib therapy for HCC is high with limited efficacy in prolonging survival. Celecoxib can inhibit the sorafenib-induced Akt activation. Celecoxib enhanced the sorafenib-induced suppression of cell proliferation, colony formation and cell migration in vitro. Celecoxib enhanced the sorafenib-induced tumor growth suppression in vivo. Long-term culture with sorafenib (1~8 months) can select sorafenib-resistant hepatoma cells. Stemness genes can be up-regulated time-dependently. Moreover, the phosphorylation of Akt was also increased. Celecoxib inhibited sorafenib resistance-promoted sphere formation, side-population and asymmetric cell division. From our study, celecoxib is a choice for HCC therapy after patient show sorafenib-resistance.
Advisors/Committee Members: hung%20Cheng%22%29&pagesize-30">Kuang-
hung Cheng (chair),
Yeu Su (chair),
Chun%20Hung%22%29&pagesize-30">Wen-Chun Hung (chair),
Ming-Hong Tai (committee member),
Tsung-Hui Hu (chair).
Subjects/Keywords: cyclooxygenase 2; sorafenib; cancer stem cells; celecoxib; hepatocellular carcinoma
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APA ·
Chicago ·
MLA ·
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CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Chu, T. (2014). Therapeutic Efficacy and Mechanism of Celecoxib for Hepatocellular Carcinoma. (Doctoral Dissertation). NSYSU. Retrieved from http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0809114-182128
Chicago Manual of Style (16th Edition):
Chu, Tian-huei. “Therapeutic Efficacy and Mechanism of Celecoxib for Hepatocellular Carcinoma.” 2014. Doctoral Dissertation, NSYSU. Accessed January 19, 2021.
http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0809114-182128.
MLA Handbook (7th Edition):
Chu, Tian-huei. “Therapeutic Efficacy and Mechanism of Celecoxib for Hepatocellular Carcinoma.” 2014. Web. 19 Jan 2021.
Vancouver:
Chu T. Therapeutic Efficacy and Mechanism of Celecoxib for Hepatocellular Carcinoma. [Internet] [Doctoral dissertation]. NSYSU; 2014. [cited 2021 Jan 19].
Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0809114-182128.
Council of Science Editors:
Chu T. Therapeutic Efficacy and Mechanism of Celecoxib for Hepatocellular Carcinoma. [Doctoral Dissertation]. NSYSU; 2014. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0809114-182128
NSYSU
19.
Chiang, Chi-Hsiang.
Regulation of microRNA-182 and its functional role in breast cancer.
Degree: PhD, Institute of Biomedical Sciences, 2013, NSYSU
URL: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0624113-191725
► MicroRNAs (MiRNAs) are endogenous small non-coding RNAs which negatively regulate gene expression by inducing translation repression or mRNA cleavage. MiR-182 is a member of the…
(more)
▼ MicroRNAs (MiRNAs) are endogenous small non-coding RNAs which negatively regulate gene expression by inducing translation repression or mRNA cleavage. MiR-182 is a member of the miR-183 cluster which is located at human chromosome 7q32 region and is over-expressed in several types of human cancer. Recent studies demonstrated that miR-182 functions as an oncogenic miRNA via inhibition of several tumor suppressor genes like FOXO3, FOXO1, BRCA1 and MTSS1. In the first part of this study, we demonstrated that miR-182 is over-expressed in human breast tumor tissues and cell lines. In addition, we found that β-catenin up-regulated miR-182 expression in breast cancer cells. Inhibition or knockdown of β-catenin significantly reduced miR-182 level in MDA-MB-231 cells. Chromatin immunoprecipitation assay confirmed the constitutive binding of β-catenin on miR-182 promoter. We further identified the tumor suppressor Reversion-inducing Cysteine-rich Protein with Kazal motifs (RECK) as a new target of miR-182. Anti-miR-182 increased RECK protein in MDA-MB-231 cells while pre-miR-182 reduced RECK protein but not mRNA in H184B5F5/M10 human normal mammary epithelial cells. Restoration of RECK protein by anti-miR-182 attenuated matrix metalloproteinase-9 (MMP-9) activity, cell invasion and colony formation. More importantly, ectopic expression of miR-182 inhibited restoration of RECK protein by β-catenin inhibitor indicating induction of miR-182 is important for β-catenin-induced down-regulation of RECK. Taken together, we provide evidences that miR-182 is up-regulated by β-catenin signaling pathway in breast cancer and its up-regulation increases MMP-9 activity and cell invasiveness by repressing RECK.
Advisors/Committee Members: Te-Hsiu Lee (chair), Jau-Shyang Huang (chair), hung%20Cheng%22%29&pagesize-30">Kuang-
hung Cheng (chair),
Yeou-Lih Huang (chair),
Wen- chun Hung (committee member).
Subjects/Keywords: RECK; β-catenin; microRNA; matrix metalloproteinase
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APA ·
Chicago ·
MLA ·
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CSE |
Export
to Zotero / EndNote / Reference
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APA (6th Edition):
Chiang, C. (2013). Regulation of microRNA-182 and its functional role in breast cancer. (Doctoral Dissertation). NSYSU. Retrieved from http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0624113-191725
Chicago Manual of Style (16th Edition):
Chiang, Chi-Hsiang. “Regulation of microRNA-182 and its functional role in breast cancer.” 2013. Doctoral Dissertation, NSYSU. Accessed January 19, 2021.
http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0624113-191725.
MLA Handbook (7th Edition):
Chiang, Chi-Hsiang. “Regulation of microRNA-182 and its functional role in breast cancer.” 2013. Web. 19 Jan 2021.
Vancouver:
Chiang C. Regulation of microRNA-182 and its functional role in breast cancer. [Internet] [Doctoral dissertation]. NSYSU; 2013. [cited 2021 Jan 19].
Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0624113-191725.
Council of Science Editors:
Chiang C. Regulation of microRNA-182 and its functional role in breast cancer. [Doctoral Dissertation]. NSYSU; 2013. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0624113-191725
NSYSU
20.
Hong, Kun-jing.
Study of the molecular mechanism by which RECK suppresses drug resistance and cancer stemness by regulating Her2/Neu and Notch oncogenic pathways.
Degree: PhD, Institute of Biomedical Sciences, 2016, NSYSU
URL: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0028116-155048
► Reversion-inducing cysteine rich protein with Kazal motifs (RECK) is an endogenous metastatic suppressor gene, which can inhibit matrix metalloproteinase MMP-2, MMP-9 and MT1-MMP to reduce…
(more)
▼ Reversion-inducing cysteine rich protein with Kazal motifs (RECK) is an endogenous metastatic suppressor gene, which can inhibit matrix metalloproteinase MMP-2, MMP-9 and MT1-MMP to reduce cancer metastasis. Clinical study showed that RECK is highly express in normal cells, but low in cancers. In general, RECK is a membrane-anchored tumor suppressor glycoprotein and correlate with the angiogenesis and metastasis in vitro and in vivo. Interesting, we found that RECK not only inhibits activity of matrix metalloproteinase, but also regulates some signaling pathways. In the first part of this study, we demonstrated that RECK inhibited Her2/Neu receptor dimerization and autophosphorylation which caused reduction of ERK and AKT kinase activity and down-regulation of Her2/Neu target genes. RECK expression is reduced in 58.8% of breast cancer tissues and is associated with lymph node invasion supporting its anti-metastatic role. In the second part, the data demonstrated that the phosphorylation of ATM and ATR pathways and γ-H2AX foci were detected in restoring the expression of RECK in breast cancer cells. RECK inhibited the Her2 signaling and attenuated the expression of the downstream molecules Jun activation domain-binding protein 1 (Jab1) and the DNA repair protein Rad51 to impede DNA repair and to increase drug sensitivity. In the third part, we selected the CD133-positive cancer stem-like cells from gastric cancer cells. Ectopic expression of RECK induced down-regulation of the expression stemness genes including Nanog, Oct4, Sox2 and the formation of cancer stem cell. In further study, RECK represses stemness gene expression and stem-like properties by inhibiting ADAM-mediated Notch1 shedding and activation. Taken together, we provide evidences that RECK regulates Her2/Neu and Notch oncogenic pathways to repress cancer cell drug resistant and tumorigenic of cancer stem cell.
Advisors/Committee Members: Te-Hsiu Lee (chair), Chun%20Hung%22%29&pagesize-30">
Wen-
Chun Hung (committee member),
Hung%20Cheng%22%29&pagesize-30">Kuang-Hung Cheng (chair),
Yeou-Lih Huang (chair),
Jau-Shyang Huang (chair).
Subjects/Keywords: RECK; glycoprotein; matrix metalloproteinase; metastasis; cancer stem cell; dimerization; autophosphorylation
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APA (6th Edition):
Hong, K. (2016). Study of the molecular mechanism by which RECK suppresses drug resistance and cancer stemness by regulating Her2/Neu and Notch oncogenic pathways. (Doctoral Dissertation). NSYSU. Retrieved from http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0028116-155048
Chicago Manual of Style (16th Edition):
Hong, Kun-jing. “Study of the molecular mechanism by which RECK suppresses drug resistance and cancer stemness by regulating Her2/Neu and Notch oncogenic pathways.” 2016. Doctoral Dissertation, NSYSU. Accessed January 19, 2021.
http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0028116-155048.
MLA Handbook (7th Edition):
Hong, Kun-jing. “Study of the molecular mechanism by which RECK suppresses drug resistance and cancer stemness by regulating Her2/Neu and Notch oncogenic pathways.” 2016. Web. 19 Jan 2021.
Vancouver:
Hong K. Study of the molecular mechanism by which RECK suppresses drug resistance and cancer stemness by regulating Her2/Neu and Notch oncogenic pathways. [Internet] [Doctoral dissertation]. NSYSU; 2016. [cited 2021 Jan 19].
Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0028116-155048.
Council of Science Editors:
Hong K. Study of the molecular mechanism by which RECK suppresses drug resistance and cancer stemness by regulating Her2/Neu and Notch oncogenic pathways. [Doctoral Dissertation]. NSYSU; 2016. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0028116-155048
NSYSU
21.
Kuo, Tzu-Lei.
Investigation of APC gene functional roles in pancreatic cancer initiation and progression.
Degree: PhD, Institute of Biomedical Sciences, 2016, NSYSU
URL: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0501116-194326
► Chapter â Adenomatous polyposis coli (APC), a tumor suppressor gene critically involved in familial adenomatous polyposis, is integral in Wnt/β-catenin signaling and is implicated in…
(more)
▼ Chapter â
Adenomatous polyposis coli (APC), a tumor suppressor gene critically involved in familial adenomatous polyposis, is integral in Wnt/β-catenin signaling and is implicated in the development of sporadic tumors of the distal gastrointestinal tract including pancreatic cancer (PC). Here we report for the first time that functional APC is required for the growth and maintenance of pancreatic islets and maturation. Subsequently, a non-Kras mutation-induced pre-malignancy mouse model was developed; in this model, APC haploinsufficiency coupled with p53 deletion resulted in the development of a distinct type of pancreatic premalignant precursors, mucinous cystic neoplasms (MCNs), exhibiting pathomechanisms identical to those observed in human MCNs, including accumulation of cystic fluid secreted by neoplastic and ovarian-like stromal cells, with 100% penetrance and the presence of hepatic and gastric metastases in > 30% of the mice. The major clinical implications of this study suggest targeting the Wnt signaling pathway as a novel strategy for managing MCN.
Chapter â¡
Pancreatic cancer is one of the most lethal malignancies due to its late diagnosis and limited response to treatment. Here, we investigate the effects of concomitant p53 and APC mutation on neoplasms initiated by oncogenic Kras in pancreas mice. In this model, APC haploinsufficiency coupled with p53 deletion and kras activation resulted in an earlier appearance of PanIN lesions and these neoplasms progressed rapidly to highly invasive and metastatic cancers. Through analysis of microarray data in mice revealed APC mutant upregulated runx3 expression and downstream target SPP1 and COL6A1 that stimulating cell migration and dissemination. We also established tumor organoid models from KPC and PKA53 mice, these organoid format multicellular invasive strands show PKA53 cell were highly invasive potential than KPC cell that identical to mice model. These comprehensive 3D cell culture model of murine PDAC progression would facilitate investigation of therapeutic targets, and diagnostics for PDAC.
Advisors/Committee Members: Li-Tzon Chen (chair), hung%20Cheng%22%29&pagesize-30">Kuang-
hung Cheng (committee member),
Chun%20Hung%22%29&pagesize-30">Wen-Chun Hung (chair),
Ko-Jiunn Liu (chair),
Yan-Shen Shan (chair).
Subjects/Keywords: Haploinsufficiency; Mucinous cystic neoplasms; p53; APC; Pancreatic cancer; metastasis; mice model; tumor organoid
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APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Kuo, T. (2016). Investigation of APC gene functional roles in pancreatic cancer initiation and progression. (Doctoral Dissertation). NSYSU. Retrieved from http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0501116-194326
Chicago Manual of Style (16th Edition):
Kuo, Tzu-Lei. “Investigation of APC gene functional roles in pancreatic cancer initiation and progression.” 2016. Doctoral Dissertation, NSYSU. Accessed January 19, 2021.
http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0501116-194326.
MLA Handbook (7th Edition):
Kuo, Tzu-Lei. “Investigation of APC gene functional roles in pancreatic cancer initiation and progression.” 2016. Web. 19 Jan 2021.
Vancouver:
Kuo T. Investigation of APC gene functional roles in pancreatic cancer initiation and progression. [Internet] [Doctoral dissertation]. NSYSU; 2016. [cited 2021 Jan 19].
Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0501116-194326.
Council of Science Editors:
Kuo T. Investigation of APC gene functional roles in pancreatic cancer initiation and progression. [Doctoral Dissertation]. NSYSU; 2016. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0501116-194326
NSYSU
22.
Chang, Tsung-ming.
Prox1 suppresses growth and metastasis of hepatocellular carcinoma by downregulating Twist1.
Degree: PhD, Institute of Biomedical Sciences, 2013, NSYSU
URL: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0110113-155844
► Prospero-related homeobox 1 (Prox1) was cloned as homeobox gene which homologous to the Drosophila prospero gene. As a transcription factor, Prox1 is important for liver…
(more)
▼ Prospero-related homeobox 1 (Prox1) was cloned as homeobox gene which
homologous to the Drosophila prospero gene. As a transcription factor, Prox1 is
important for liver development and is highly expressed in adult hepatocytes. In
contrast, down-regulation of Prox1 in hepatocellular carcinoma (HCC) is associated
with poor differentiation, prognosis, and reduced overall survival which implying a
potential tumor suppressive role of Prox1 in HCC. However, the molecular
mechanisms of Prox1âs tumor suppressive function are still obscure. In this study, we
find that Prox1 expression is positively associated with E-cadherin and negatively
linked with Twist1 and vimentin in various HCC cell lines. Ectopic expression of
Prox1 reduces Twist1 while knockdown of Prox1 increased Twist1 expression. We
further identify a putative Prox1 binding site located at the -117/-111 bp of the Twist1
promoter which is critical for gene repression. Chromatin immunoprecipitation assays
also demonstrate the direct binding of Prox1 to human Twist1 promoter. In addition,
inhibition of Twist1 by Prox1 causes p53 up-regulation and AKT2 down-regulation.
Moreover, functional assays show that wild-type p53 induction is important for the
growth-inhibitory effect of Prox1 and AKT2 is involved in the inhibition of migration
and invasion by Prox1. In consistence with the results of cell-based study, animal
experiments demonstrate that Prox1 significantly attenuates tumor growth and lung
metastasis in vivo. Collectively, we conclude that Prox1 functions as a tumor
suppressor in HCC cells via inhibiting Twist1 to trigger p53-dependent
senescence-like phenotype and to reduce AKT2-mediated invasion.
Advisors/Committee Members: Yeou-Lih Huang (chair), Chun%20Hung%22%29&pagesize-30">
Wen-
Chun Hung (committee member),
Ching-Shuang Wu (chair),
Long-Sen Chang (chair),
hung%20Cheng%22%29&pagesize-30">Kuang-hung Cheng (chair).
Subjects/Keywords: AKT2; p53; Prox1; Twist1
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APA ·
Chicago ·
MLA ·
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Manager
APA (6th Edition):
Chang, T. (2013). Prox1 suppresses growth and metastasis of hepatocellular carcinoma by downregulating Twist1. (Doctoral Dissertation). NSYSU. Retrieved from http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0110113-155844
Chicago Manual of Style (16th Edition):
Chang, Tsung-ming. “Prox1 suppresses growth and metastasis of hepatocellular carcinoma by downregulating Twist1.” 2013. Doctoral Dissertation, NSYSU. Accessed January 19, 2021.
http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0110113-155844.
MLA Handbook (7th Edition):
Chang, Tsung-ming. “Prox1 suppresses growth and metastasis of hepatocellular carcinoma by downregulating Twist1.” 2013. Web. 19 Jan 2021.
Vancouver:
Chang T. Prox1 suppresses growth and metastasis of hepatocellular carcinoma by downregulating Twist1. [Internet] [Doctoral dissertation]. NSYSU; 2013. [cited 2021 Jan 19].
Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0110113-155844.
Council of Science Editors:
Chang T. Prox1 suppresses growth and metastasis of hepatocellular carcinoma by downregulating Twist1. [Doctoral Dissertation]. NSYSU; 2013. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0110113-155844
NSYSU
23.
Cheng, Hsueh-Tsen.
Anti-lymphangiogenic action of SAHA on breast cancer.
Degree: PhD, Institute of Biomedical Sciences, 2013, NSYSU
URL: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0403113-151923
► HDAC inhibitor suberoylanilide hydroxamic acid (SAHA) exhibits anti-tumor effects on various types of human cancers and is now approved by U.S FDA for clinical cancer…
(more)
▼ HDAC inhibitor suberoylanilide hydroxamic acid (SAHA) exhibits anti-tumor effects on various types of human cancers and is now approved by U.S FDA for clinical cancer treatment. SAHA also suppresses tumor angiogenesis. However, the effect of SAHA on tumor lymphangiogeneis is unclear. My study focuses on anti-lymphangiogenic action of SAHA on breast cancers and contains three parts. In part one, I test whether SAHA affects the production of pro-lymphangiogenesis factor such as VEGF-C to reduce proliferation and migration of lymphatic endothelial cells toward cancer cells. I found that SAHA does-dependently inhibited the expression of VEGF-C in various breast cancer cell lines and the secretion of VEGF-C into conditioned medium was also suppressed. Furthermore, I cloned human VEGF-C gene promoter and demonstrated that SAHA directly suppressed VEGF-C transcription via the -185/+38 promoter region in a Sp1-mediated manner.
In part two, I aim to study the effect of SAHA on lymphatics endothelial cells (LECs). I established a lymphatic-like endothelial cell line (named as FP01) by overexpressing the master LEC transcription factor PROX1 in EA.hy926 endothelial cells. This cell lines showed similar gene expression pattern and phenotype of primarily cultured LECs. I found that SAHA can suppress proliferation, sprouting and tube formation of LECs. Moreover, SAHA could attenuate the angiopoietin/Tie signaling pathway which is important in the regulation of LEC function. The promoter activity assay revealed that SAHA down-regulated the expression of Tie2 through transcriptional repression. Interestingly, I also found that SAHA could quickly induce the expression of c-Cbl, the E3 ligase for Tie2 ubiquitination leading to Tie2 protein degradation. Knockdown of c-Cbl effectively reversed SAHA-induced Tie2 protein degradation.
In part three, I used breast cancer xenograft model to demonstrate whether SAHA could repress lymphangiogenesis and lymphatic metastasis in vivo. SAHA indeed inhibited tumor formation, lymphangiogenesis and metastasis in MDA-MB-231 luciferase-tagged xenograft model.
Taken together, SAHA not only suppresses proliferation, sprouting and tube formation of LECs and attenuates the Ang/Tie signaling in LECs by down-regulating Tie2 via transcriptional and post-transcriptional mechanism but also inhibits VEGF-C expression in breast cancer cells via transcriptional repression. Breast cancer xenograft model demonstrates that SAHA inhibits tumor formation, lymphangiogenesis and metastasis in vivo. Collectively, this drug exerts anti-lymphangiogenic activity in cancer treatment.
Advisors/Committee Members: Te-Hsiu Lee (chair), Jau-Shyang Huang (chair), hung%20Cheng%22%29&pagesize-30">Kuang-
hung Cheng (chair),
Yeou-Lih Huang (chair),
Chun%20Hung%22%29&pagesize-30">Wen-Chun Hung (committee member).
Subjects/Keywords: HDAC inhibitor SAHA; lymphangiogenesis; breast cancer; VEGF-C; c-Cbl
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APA ·
Chicago ·
MLA ·
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CSE |
Export
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APA (6th Edition):
Cheng, H. (2013). Anti-lymphangiogenic action of SAHA on breast cancer. (Doctoral Dissertation). NSYSU. Retrieved from http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0403113-151923
Chicago Manual of Style (16th Edition):
Cheng, Hsueh-Tsen. “Anti-lymphangiogenic action of SAHA on breast cancer.” 2013. Doctoral Dissertation, NSYSU. Accessed January 19, 2021.
http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0403113-151923.
MLA Handbook (7th Edition):
Cheng, Hsueh-Tsen. “Anti-lymphangiogenic action of SAHA on breast cancer.” 2013. Web. 19 Jan 2021.
Vancouver:
Cheng H. Anti-lymphangiogenic action of SAHA on breast cancer. [Internet] [Doctoral dissertation]. NSYSU; 2013. [cited 2021 Jan 19].
Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0403113-151923.
Council of Science Editors:
Cheng H. Anti-lymphangiogenic action of SAHA on breast cancer. [Doctoral Dissertation]. NSYSU; 2013. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0403113-151923
NSYSU
24.
Tsai, Han-en.
The Therapeutic Potential and Mechanism of POMC stress Hormone for Metastatic Cancer.
Degree: PhD, Institute of Biomedical Sciences, 2012, NSYSU
URL: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0823112-163353
► Despite the development of novel target therapy drugs in recent years, metastatic cancer remains refractory to current cancer therapies and accounts for the majority of…
(more)
▼ Despite the development of novel target therapy drugs in recent years, metastatic cancer remains refractory to current cancer therapies and accounts for the majority of cancer mortalities worldwide. Metastasis consists of multiple steps including angiogenesis, extravasion, escape from immune surveillance, adhesion, and clonal expansion in different organs that a systemic therapy is required for effective control of metastasis. The pro-inflammatory nuclear factor kappa B (NFκB) pathway plays an important role during each of these metastatic events and constitutes an excellent target for metastasis control. Stress hormone pro-opiomelanocortin (POMC) and its derived neuropeptides including corticotrophin (ACTH), α-, β-, and γ-melanocyteâstimulating hormone (α-, β-, and γ-MSH), β-endorphin are potent inhibitors of NFκB pathway. Other than the central regulation of stress response and energy homeostasis, POMC also regulates the skin pigmentation, inflammatory processes, and immune reactions in the peripheral system. Since adenovirusâmediated POMC gene delivery leads to hepatic POMC expression, it seems plausible that POMC gene therapy may elicit systemic production of anti-inflammatory POMC-derived peptides and hold promises for control of primary and metastatic cancers. In B16-F10 melanoma models, POMC gene delivery elevated the circulating ACTH levels for more than 8 weeks and suppressed the growth of established melanoma, thereby prolonging the life span of tumor-bearing mice. Moreover, combination of POMC therapy with cisplatin further enhances the survival outcome. Subsequent analysis reveals that POMC gene therapy inhibits the growth and metastasis of melanoma through apoptosis, angiogenesis inhibition, and modulation of epithelial-mesenchymal transition. Besides, α-MSH/melanortin-1 receptor (MC-1R) pathway is involved in the POMC-mediated melanoma suppression.
To investigate whether POMC therapy could be applied to other types of tumor, we evaluated the therapeutic efficacy of POMC gene therapy in Lewis lung carcinoma (LLC) cells which lack MC-1R. Interestingly, POMC gene delivery effectively inhibited the proliferation and colony formation of LLC cells in vitro and the growth of established LLC in mice. Histological analysis indicated that POMC gene delivery attenuated LLC through proliferation inhibition, apoptosis induction, and angiogenesis blockade. Moreover, POMC gene delivery perturbed β-catenin signaling by reducing protein levels of β-catenin and its downstream proto-oncogenes, including cyclin D1 and c-myc. These results support the existence of an MC-1R-independent pathway for POMC gene therapy and expand the therapeutic spectrum of POMC therapy for multiple types of cancer.
To elucidate the role of host immunity in anti-neoplastic mechanism underlying POMC therapy, we compared the treatment efficacy of POMC gene therapy for B16-F10 melanoma between severe combined immune-deficient (SCID) and immune-competent C57BL/6 mice, and found similar extent of tumor suppression in both strains of mice.…
Advisors/Committee Members: Long-sen Chang (chair), Chun%20Hung%22%29&pagesize-30">
Wen-
Chun Hung (chair),
Ming-Hong Tai (committee member),
Po-Lin Kuo (chair),
Hung%20Cheng%22%29&pagesize-30">Kuang-Hung Cheng (chair).
Subjects/Keywords: Gene Therapy; Immune system; POMC; Metastasis; Melanoma; Epithelial-mesenchymal transition
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APA ·
Chicago ·
MLA ·
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CSE |
Export
to Zotero / EndNote / Reference
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APA (6th Edition):
Tsai, H. (2012). The Therapeutic Potential and Mechanism of POMC stress Hormone for Metastatic Cancer. (Doctoral Dissertation). NSYSU. Retrieved from http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0823112-163353
Chicago Manual of Style (16th Edition):
Tsai, Han-en. “The Therapeutic Potential and Mechanism of POMC stress Hormone for Metastatic Cancer.” 2012. Doctoral Dissertation, NSYSU. Accessed January 19, 2021.
http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0823112-163353.
MLA Handbook (7th Edition):
Tsai, Han-en. “The Therapeutic Potential and Mechanism of POMC stress Hormone for Metastatic Cancer.” 2012. Web. 19 Jan 2021.
Vancouver:
Tsai H. The Therapeutic Potential and Mechanism of POMC stress Hormone for Metastatic Cancer. [Internet] [Doctoral dissertation]. NSYSU; 2012. [cited 2021 Jan 19].
Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0823112-163353.
Council of Science Editors:
Tsai H. The Therapeutic Potential and Mechanism of POMC stress Hormone for Metastatic Cancer. [Doctoral Dissertation]. NSYSU; 2012. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0823112-163353
NSYSU
25.
Weng, Ching-Chieh.
Investigation of TGF-β repressors inactivation enhances metastasis in Pancreatic cancer.
Degree: PhD, Institute of Biomedical Sciences, 2018, NSYSU
URL: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0624118-181253
► The overall five-year survival rate for pancreatic cancer reported as low as 5% a decade ago, even now still less than 10%. The main issue…
(more)
▼ The overall five-year survival rate for pancreatic cancer reported as low as 5% a decade ago, even now still less than 10%. The main issue in pancreatic cancer is patients in the early stages of pancreatic cancer have no obvious symptoms which leads to be diagnosed almost delay to advanced stages when patients harbored abdominal pain, jaundice or ascites. To explore what makes pancreatic cancer becoming highly invasive and metastatic may prolong survival for pancreatic cancer patients. Several studies have demonstrated that the increased TGF-β secretion in the tumor microenvironment may associate with the survival and poor prognosis of pancreatic cancer patients. Importantly, Smad4, a member of the SMAD family of signaling transduction, which acts as a pivotal mediator of TGF-β, was identified to be inactivated in more than 50% of pancreatic cancer. Alternatively, inactivation of the downstream factors in the TGF-β/SMAD signaling pathway may also affect the development of pancreatic. My thesis work is divided into two parts, the first part of the thesis is to investigate the effect of Krueppel-like factor 10 (KLF10), also named TGFβ-inducible early growth response protein 1(TIEG-1) on pancreas development and pancreatic cancer progression. We demonstrated that conditional KLF10 deletion in the pancreatic epithelium had no discernable impact on pancreatic development or physiology. However, when combined with the activated KRASG12D allele, KLF10 loss enabled rapid progression of KRASG12D âinduced tumorigenesis. While activation of KRASG12D alone elicited premalignant pancreatic intraepithelial neoplasia (PanIN) that progressed slowly to high grades of PanINs, the combination of KRASG12D and KLF10 deficiency resulted in the rapid development of tumors resembling pancreatic ductal adenocarcinoma (PDAC) in humans. KLF10 loss also accelerated PDAC development of KRASG12DP53L/L compound mice and altered the prometastatic phenotype by involving the activation of SDF-1/CXCR4 stemness pathway. In the second part of my study, we investigate another TGFβ1/SMAD downstream repressor TGFβ-induced factor homeobox 1 (TGIF1) to study the potential role of TGIF1 in PDAC development. We selective deleted TGIF1, by using Cre-Loxp system to cross with Pdx-1Cre KrasG12D and Pdx-1CreKRASG12D P53L/L models in order to clarify the impact of TGIF1 deletion on malignant progression of PDAC. We observed that Pdx-1CreKRASG12DTGIF1L/LP53L/L PDAC model displayed the high frequency of lung and liver metastasis during PDAC formation in mutant mice. We further revealed that TGIF1 loss contributed to the progression of KRASG12D-induced PDAC through activation of HAS2-CD44 signaling pathway and upregulation of PDL1. Lastly, our results suggested that these KLF10-TGIF1 involving signaling networks might potentially become new therapeutic nodes for the treatment of pancreatic cancer metastasis.
Advisors/Committee Members: Hung%20Cheng%22%29&pagesize-30">Kuang-
Hung Cheng (committee member),
Li-Tzong Chen (chair),
Chien-Feng Li (chair),
Jim Jinn-Chyuan Sheu (chair),
Chun%20Hung%22%29&pagesize-30">Wen-Chun Hung (chair).
Subjects/Keywords: KLF10; Pancreatic cancer; PDAC mouse model; TGIF1; Metastasis
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APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Weng, C. (2018). Investigation of TGF-β repressors inactivation enhances metastasis in Pancreatic cancer. (Doctoral Dissertation). NSYSU. Retrieved from http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0624118-181253
Chicago Manual of Style (16th Edition):
Weng, Ching-Chieh. “Investigation of TGF-β repressors inactivation enhances metastasis in Pancreatic cancer.” 2018. Doctoral Dissertation, NSYSU. Accessed January 19, 2021.
http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0624118-181253.
MLA Handbook (7th Edition):
Weng, Ching-Chieh. “Investigation of TGF-β repressors inactivation enhances metastasis in Pancreatic cancer.” 2018. Web. 19 Jan 2021.
Vancouver:
Weng C. Investigation of TGF-β repressors inactivation enhances metastasis in Pancreatic cancer. [Internet] [Doctoral dissertation]. NSYSU; 2018. [cited 2021 Jan 19].
Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0624118-181253.
Council of Science Editors:
Weng C. Investigation of TGF-β repressors inactivation enhances metastasis in Pancreatic cancer. [Doctoral Dissertation]. NSYSU; 2018. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0624118-181253
NSYSU
26.
Yang, Kuei-Ting.
Regulation of Jab1 by Bcr-Abl Oncogene.
Degree: Master, Institute of Biomedical Sciences, 2007, NSYSU
URL: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0816107-112047
► The COP9 signalosome (CSN) contains eight-subunits and is a highly conserved protein complex implicated in ubiquitin-mediated proteolysis. Jun activation domain-binding protein 1 (Jab1) is the…
(more)
▼ The COP9 signalosome (CSN) contains eight-subunits and is a highly conserved protein complex implicated in ubiquitin-mediated proteolysis. Jun activation domain-binding protein 1 (Jab1) is the fifth component of CSN (CSN5) with a molecular weight of 38 kDa. Jab1 overexpression is observed in many human cancers, but there is no clear evidence how Jab1 contributes to malignant transformation in human cancers. Bcr-Abl is a cytoplasmic chimeric oncoprotein produced by Philadelphia chromosome
translocation and found in more than 90% of patients with chronic myelogenous leukemia (CML). Recent studies have shown that the Jab1/COP9 signalosome subcomplex is a downstream mediator of Bcr-Abl kinase and may facilitate cell-cycle progression. In this study, we found that inhibition of Bcr-Abl kinase by STI-571 downregulated 50% of full length human Jab1 promoter activity and gene expression. Promoter deletion assay indicated that the responsive element for Bcr-Abl is located between -405/-223 region of human Jab1 promoter. Treatment of LY294002 also reduced Jab-405/-223 promoter activity and Jab1
expression. Promoter mutagenesis assay and ChIP assay suggest that Bcr-Abl stimulated both β-catenin /TCF complex and STAT1 bind to the consensus binding sites of Jab-405/-223 promoter. Taken together, Bcr-Abl oncogene may regulate Jab1 via PI3K/AKT signal pathway, β-catenin /TCF and STAT1 transcription factors.
Advisors/Committee Members: Hui-Chiu Chang (chair), Yow-Ling Shiue (chair), Chun%20Hung%22%29&pagesize-30">
Wen-
Chun Hung (committee member).
Subjects/Keywords: Bcr-Abl; CML; Jab1
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APA (6th Edition):
Yang, K. (2007). Regulation of Jab1 by Bcr-Abl Oncogene. (Thesis). NSYSU. Retrieved from http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0816107-112047
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Yang, Kuei-Ting. “Regulation of Jab1 by Bcr-Abl Oncogene.” 2007. Thesis, NSYSU. Accessed January 19, 2021.
http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0816107-112047.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Yang, Kuei-Ting. “Regulation of Jab1 by Bcr-Abl Oncogene.” 2007. Web. 19 Jan 2021.
Vancouver:
Yang K. Regulation of Jab1 by Bcr-Abl Oncogene. [Internet] [Thesis]. NSYSU; 2007. [cited 2021 Jan 19].
Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0816107-112047.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Yang K. Regulation of Jab1 by Bcr-Abl Oncogene. [Thesis]. NSYSU; 2007. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0816107-112047
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
NSYSU
27.
Chen, Bo-rong.
Role of insulin resistance in nucleus tractus solitarii on central cardiovascular regulation in rats.
Degree: Master, Institute of Biomedical Sciences, 2007, NSYSU
URL: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0723107-143624
► Insulin resistance was thought as the major etiology of hypertension of the metabolic syndrome. Both human and animal studies revealed sympathetic overactivity were present in…
(more)
▼ Insulin resistance was thought as the major etiology of hypertension of the metabolic syndrome. Both human and animal studies revealed sympathetic overactivity were present in the metabolic syndrome. Nowadays, most of the studies that examined the etiologies of hypertension of metabolic syndrome were focused on the pathophysiologic effects of insulin resistance on the peripheral vessels. However, there was no study ever examined the insulin resistance in cardiovascular regulatory centers of central nervous system or the pathogenesis of sympathetic overactivity in metabolic syndrome. Our previous study demonstrated that insulin plays a cardiovascular regulatory role in the nucleus tractus solitarii (NTS), one of the cardiovascular regulatory centers in the brain stem. We also demonstrated that the cardiovascular regulatory effects of insulin in the NTS were accomplished through activating PI3K-PKB/Akt-NO signaling pathways. Recently, increases in oxidative stress could raise the incidence rate of diabetes mellitus and cardiovascular diseases had been reported. Besides, it has been reported that there were marked increases in reactive oxidative species (ROS) in various hypertension animal models. It was also reported that elevation of ROS in various tissues may activate the mitogen-activated protein kinase (MAPK) superfamily. Activated MAPKs may phosphorylate insulin receptor substrate 1 (IRS1) on the serine 307 residue. It has been reported that IRS1S307 phosphorylation would inhibit normal insulin signal transduction. The aims of this thesis were to investigate whether the neuronal cells in the NTS would develop insulin resistance in the metabolic syndrome rats, whether development of insulin resistance in the NTS cause hypertension in the metabolic syndrome rats, which signaling molecule in insulin signaling pathway is the key molecule that cause insulin resistance in the NTS, and what the pathogenesis of insulin resistance is in the NTS of metabolic syndrome rats. In the pioneer study, Wistar-Kyoto (WKY) rats were fed with 10% fructose water as their drinking water for 8 weeks. Another group of fructose-fed WKY rats were fed with insulin sensitizer, rosiglitazone, since the 5th week. Blood pressure was measured by tail vein sphygmomanometer every week and venous blood were draw to measure blood sugar and insulin level every other week. Thereafter, all the rats enrolled in this study were fed with 10% fructose water with/without rosiglitazone for 2-3 weeks. My results demonstrated the blood pressure of fructose-fed WKY rats was significantly elevated after 2-week fructose feeding. But at the same time, HOMA-IR did not elevated, which indicated the insulin resistance in the peripheral did not develop yet. Interestingly, at the same time, endogenous insulin in the NTS was significantly elevated in the fructose-fed group. The cardiovascular responses of insulin in the NTS were diminished in the fructose-fed group. While in the rosiglitazone-treated group, the blood pressure and endogenous insulin in the NTS were…
Advisors/Committee Members: Ching-Jiunn Tseng (committee member), Chun%20Hung%22%29&pagesize-30">
Wen-
Chun Hung (chair),
Hsiao, Michael (chair),
Pei-Jung Lu (chair).
Subjects/Keywords: hypertension; nucleus tractus solitarii; insulin resistance
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APA ·
Chicago ·
MLA ·
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CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Chen, B. (2007). Role of insulin resistance in nucleus tractus solitarii on central cardiovascular regulation in rats. (Thesis). NSYSU. Retrieved from http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0723107-143624
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Chen, Bo-rong. “Role of insulin resistance in nucleus tractus solitarii on central cardiovascular regulation in rats.” 2007. Thesis, NSYSU. Accessed January 19, 2021.
http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0723107-143624.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Chen, Bo-rong. “Role of insulin resistance in nucleus tractus solitarii on central cardiovascular regulation in rats.” 2007. Web. 19 Jan 2021.
Vancouver:
Chen B. Role of insulin resistance in nucleus tractus solitarii on central cardiovascular regulation in rats. [Internet] [Thesis]. NSYSU; 2007. [cited 2021 Jan 19].
Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0723107-143624.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Chen B. Role of insulin resistance in nucleus tractus solitarii on central cardiovascular regulation in rats. [Thesis]. NSYSU; 2007. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0723107-143624
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
NSYSU
28.
Yen, Yi-Chen.
Molecular Interaction of Tau and Microtubule.
Degree: Master, Institute of Biomedical Sciences, 2002, NSYSU
URL: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0821102-151102
► Tau protein is one of the microtubule-associated proteins (MAPs) and mainly expressed in neuronal cells. It hasbeen demonstrated that Tau may play an important role…
(more)
▼ Tau protein is one of the microtubule-associated proteins (MAPs) and mainly expressed in neuronal cells. It hasbeen demonstrated that Tau may play an important role in regulating microtubule dynamic in neurons. Structurally and functionally, Tau protein composed of regulatory projection domain in N-terninus and microtubule-binding domain in C-terminus. It has been shown that the biological function of Tau protein was regulated by phosphorylation and dephosphorylation. In Alzheimerâs disease (AD) brain, hyperphosphorylated Tau caused by over active kinases may contribute to the disassociation of Tau from microtubule and form the pathologically hallmarker, paired helical filaments (PHFs). The reason to study cdc2 and GSK3β is two folds. First, both cdc2 and GSK3β activities are raised abbrently in AD brain. Second, the phosphorylation sites of cdc2 and GSK3β have been identified as those in PHFs.These prompted us to regard cdc2 and GSK3β as candidates that hyperphosphorylated Tau in AD.
In the following study, we used immunofluorescence analysis, co-immunoprecipitation and GST-fusion protein pull down assay to clarify the subcellular localization of Tau. We also shown that the interaction between tubulin withfull length Tau (Tau WT) and some Tau mutants that we found that not only Tau WT, but also N-terminus of Tau (Tau-N) and C-terminus of Tau (Tau-C) can bind to tubulin. Surprisingly, we observed that a fragment of N-terminus, Tau 122-244, localized in nucleus. Furthermore, we used tubulin assembly assay to test if tau or its mutants can promote tubulin assembly in vitro. Results showed that only Tau WT can promote tubulin assembly in vitro but not Tau-N or Tau-C. Although Tau-N or Tau-C can bind to tubulin in vivo and in vitro, these mutants did not remain the ability to promote tubulin assembly that suggested both functional domains, N-terminus and C-terminus of Tau, are necessary and essential for the biological function of Tau. On the other hand, we used of phosphorylation assay and site directed mutagenesis to demonstrate that T231 of Tau is one of important phosphorylation sites of cdc2 and GSK3β. Finally, we used tubulin assembly assay to show that phosphorylated Tau by GSK3β can negatively regulate the ability of Tau to promote tubulin assembly that indicated that the phosphorylation at T231 may play a role in regulating Tau.
Advisors/Committee Members: Pei-Jung Lu (committee member), Jiin-Tsuey Cheng (chair), Chun%20Hung%22%29&pagesize-30">
Wen-
Chun Hung (chair).
Subjects/Keywords: phosphorylation; tau protein; microtubule
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Yen, Y. (2002). Molecular Interaction of Tau and Microtubule. (Thesis). NSYSU. Retrieved from http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0821102-151102
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Yen, Yi-Chen. “Molecular Interaction of Tau and Microtubule.” 2002. Thesis, NSYSU. Accessed January 19, 2021.
http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0821102-151102.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Yen, Yi-Chen. “Molecular Interaction of Tau and Microtubule.” 2002. Web. 19 Jan 2021.
Vancouver:
Yen Y. Molecular Interaction of Tau and Microtubule. [Internet] [Thesis]. NSYSU; 2002. [cited 2021 Jan 19].
Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0821102-151102.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Yen Y. Molecular Interaction of Tau and Microtubule. [Thesis]. NSYSU; 2002. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0821102-151102
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
NSYSU
29.
Chen, Chia-Yi.
Divalent cation-induced conformational changes and oligomerization of KChIP1.
Degree: Master, Institute of Biomedical Sciences, 2003, NSYSU
URL: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0619103-133648
Subjects/Keywords: KChIP; conformational change; oligomerization
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APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Chen, C. (2003). Divalent cation-induced conformational changes and oligomerization of KChIP1. (Thesis). NSYSU. Retrieved from http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0619103-133648
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Chen, Chia-Yi. “Divalent cation-induced conformational changes and oligomerization of KChIP1.” 2003. Thesis, NSYSU. Accessed January 19, 2021.
http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0619103-133648.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Chen, Chia-Yi. “Divalent cation-induced conformational changes and oligomerization of KChIP1.” 2003. Web. 19 Jan 2021.
Vancouver:
Chen C. Divalent cation-induced conformational changes and oligomerization of KChIP1. [Internet] [Thesis]. NSYSU; 2003. [cited 2021 Jan 19].
Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0619103-133648.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Chen C. Divalent cation-induced conformational changes and oligomerization of KChIP1. [Thesis]. NSYSU; 2003. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0619103-133648
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
NSYSU
30.
Cheng, Yun-Ching.
Cloning and functional expression of Taiwan cobra chymotrypsin inhibitor.
Degree: Master, Institute of Biomedical Sciences, 2003, NSYSU
URL: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0620103-142902
► Previous studies showed that dendrotoxins and B chain of b-Bungarotoxin shared sequence and structural homology with Kunitz-type protease inhibitors. In the present study, the cDNA…
(more)
▼ Previous studies showed that dendrotoxins and B chain of b-Bungarotoxin shared sequence and structural homology with Kunitz-type protease inhibitors. In the present study, the cDNA of Kunitzâtype protease inhibitor was successfully amplified from Taiwan cobra venom gland total RNAs using the primers designed from the B chain of b-Bungarotoxin. The deduced amino acid sequence of the cDNA exhibited the structural character of chymotrypsin inhibitor, and the mature protein contained 57 amino acids with six Cys residues. The chymotrypsin inhibitor was subcloned into pET29a(+) and transformed into BL21(DE3) E.coli strain. The expressed protein was isolated from inclusion bodies of E.coli and subjected to refolding into its folded structure. The inhibitor potency of the recombinant protein on chymotrypsin activity had a Ki value of 461.3 mM. However, removal of its N-terminal fused peptide with thrombin further increased the Ki value to 31.7 mM. Removal of the N-terminal residues further reduced its inhibitory potency, and the inhibitory activity completely lost after deleting three residues at the N-terminus of mature protein. This reflects that the N-terminal region of protease inhibitor should be associated with its activity. The genomic DNA encoding the precursor of the inhibitor was also amplified using PCR. The genetic structure composed of three exons and three introns, which shared the same organization with the b-Bungarotoxin B chain gene. Moreover, the two genes showed a high degree of sequence identity up to 83%. This observation emphasizes the idea that the B chain of b-Bungarotoxin and protease inhibitor are evolutionarily related.
Advisors/Committee Members: Chun-Chang Chang (chair), Leng-Sen Chang (committee member), Chun%20Hung%22%29&pagesize-30">
Wen-
Chun Hung (chair).
Subjects/Keywords: taiwan cobra; chymotrypsin inhibitor
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Cheng, Y. (2003). Cloning and functional expression of Taiwan cobra chymotrypsin inhibitor. (Thesis). NSYSU. Retrieved from http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0620103-142902
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Cheng, Yun-Ching. “Cloning and functional expression of Taiwan cobra chymotrypsin inhibitor.” 2003. Thesis, NSYSU. Accessed January 19, 2021.
http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0620103-142902.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Cheng, Yun-Ching. “Cloning and functional expression of Taiwan cobra chymotrypsin inhibitor.” 2003. Web. 19 Jan 2021.
Vancouver:
Cheng Y. Cloning and functional expression of Taiwan cobra chymotrypsin inhibitor. [Internet] [Thesis]. NSYSU; 2003. [cited 2021 Jan 19].
Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0620103-142902.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Cheng Y. Cloning and functional expression of Taiwan cobra chymotrypsin inhibitor. [Thesis]. NSYSU; 2003. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0620103-142902
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
◁ [1] [2] ▶
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Open Access Theses and Dissertations