You searched for +publisher:"NSYSU" +contributor:("Chih-Wen Shu").
Showing records 1 – 7 of
7 total matches.
No search limiters apply to these results.
NSYSU
1.
Liu, Yen-Chen.
Probiotics attenuated Salmonella-induced Intestinal Inflammation via TGF-β/Smads signaling.
Degree: Master, Biological Sciences, 2013, NSYSU
URL: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0802113-175919 
► Human intestine contains a dense and diverse community of microorganisms. Normal intestinal microflora comprises an estimated 400 different bacterial species, including probiotics and pathogens; these…
(more)
▼ Human intestine contains a dense and diverse community of microorganisms. Normal intestinal microflora comprises an estimated 400 different bacterial species, including probiotics and pathogens; these microbes collectively referred to as the commensal microflora, have an important role in human nutrition and health. Salmonella is a common pathogen during summer in Taiwan. The symptoms of salmonellosis include acute responses, such as nausea, vomiting, abdominal pain, diarrhea, even death, and chronic inflammatory response, such as lymphoid depletion and necrotizing ileitis in the intestine.
TGF-β (Transforming growth factor β)-phosphorizates and activates Smad2/3 to increase IκBα (nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor), subsequently reduces inflammatory factors, such as NF-κB (Nuclear Factor-kappa B), TNF-α (tumor necrosis factor α) and IL-8 (interleukin 8) expression. Further, Smad 7 negatively regulates TGF-β signaling pathway to augment inflammation. In this study, probiotics (Lactobacillus acidophilus) and Salmonella, and human intestinal Caco-2 cells were employed to investigate how probiotics attenuates Salmonella-mediated intestinal inflammation. The results showed that Salmonella infection induced maximal NF-κB expression and TNF-α secretion at the concentrations of 107 CFU/ml; however, probiotics-pretreated cells had significantly lower TNF-α and NF-κB than those with Salmonella infection alone (p<0.05). They also had relatively higher activity of TGF-β/Samd3/4 (p<0.05). Moreover, IκBα expression in probiotics-pretreated cells was higher than that of S. typhimurium infection alone, but Smad 7 expression was lower in probiotics-pretreated cells. Consistent with Smad7 expression, miR-21, a down-regulator of Smad 7, was significantly higher in probiotics and synbiotics-pretreated cells compared with that of S. typhimurium infection alone. The experimental results showed that probiotics effectively attenuated Salmonella-induced intestinal inflammation in human intestinal Caco-2 cells via TGF-β1/Smads and TGF-β1/miR21 signaling pathway.
Advisors/Committee Members: Wen%20Shu%22%29&pagesize-30">
Chih-
Wen Shu (chair),
Jong-Kang Liu (committee member),
Pei-Feng Liu (chair),
I-Fei Huang (committee member).
Subjects/Keywords: Smads; transforming growth factor β; Probiotics; Nuclear Factor-kappa B; IL-8; Salmonella
Record Details
Similar Records
Cite
Share »
Record Details
Similar Records
Cite
« Share
❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Liu, Y. (2013). Probiotics attenuated Salmonella-induced Intestinal Inflammation via TGF-β/Smads signaling. (Thesis). NSYSU. Retrieved from http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0802113-175919
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, Yen-Chen. “Probiotics attenuated Salmonella-induced Intestinal Inflammation via TGF-β/Smads signaling.” 2013. Thesis, NSYSU. Accessed April 16, 2021.
http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0802113-175919.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Liu, Yen-Chen. “Probiotics attenuated Salmonella-induced Intestinal Inflammation via TGF-β/Smads signaling.” 2013. Web. 16 Apr 2021.
Vancouver:
Liu Y. Probiotics attenuated Salmonella-induced Intestinal Inflammation via TGF-β/Smads signaling. [Internet] [Thesis]. NSYSU; 2013. [cited 2021 Apr 16].
Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0802113-175919.
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. Probiotics attenuated Salmonella-induced Intestinal Inflammation via TGF-β/Smads signaling. [Thesis]. NSYSU; 2013. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0802113-175919
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
NSYSU
2.
Li, Yi-jing.
LC3, P62, P65, and EGFR Protein Expressions are Associated with Tumor Transformation and Poor Prognosis in Oral Squamous Cell Carcinoma.
Degree: Master, Biological Sciences, 2016, NSYSU
URL: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0621116-000801
► Oral cancer, a common type of head and neck cancer, is the sixth most common malignant tumors in the world. Tongue, buccal mucosa, and lip…
(more)
▼ Oral cancer, a common type of head and neck cancer, is the sixth most common malignant tumors in the world. Tongue, buccal mucosa, and lip are the top three most common subsites of oral cavity. Autophagy plays an important role on tumor growth and progression in many cancers. Upregulation of autophagy in cancer can be either prosurvival or prodeath for tumor cells. The associations of expression levels of LC3, p62, p65, and EGFR with the tumorigenesis, clinicopathologic outcomes, and survival for three primary subsites of oral cancer were investigated. A total of 498 oral squamous cell carcinoma (OSCC) patients were recruited, including 181 buccal mucosal SCC (BMSCC), 244 tongue SCC (TSCC), and 73 lip SCC (LSCC) patients. In addition, another 76 sleep apnea patients for uvula excision were also recruited as controls. The expression levels of LC3, p62, p65 in the nuclear, p65 in the cytoplasm , EGFR in the Membrane (EGFR-M) and EGFR in the cytoplasm (EGFR-C) in three kinds of tissues, including normal, tumor, and corresponding tumor adjacent normal (TAN) were evaluated by immunohistochemistry using tissue microarray. An increased expression of LC3, p62, p65-C, EGFR-M, and EGFR-C was found in OSCC tissues and three subsites as compared to those in TAN and normal tissues (all p<0.001). However, p65-N expression was found significantly decreased in OSCC (all p<0.002), except in LSCC (p=0.119). In BMSCC patients, the higher expression of p62 was associated with poor cell differentiation (p=0.015) and lymph node metastasis (p=0.033). However, the expression of EGFR in N0 was higher than that in lymph node metastasis (p=0.031). In TSCC patients, the higher expressions of LC3 (p=0.045), p62 (p=0.040), and p65-C (p<0.001) were associated with poor cell differentiation. Moreover, higher expressions of EGFR-C are associated with advanced AJCC pathological stage (p<0.001), higher T classification (p=0.003), and lymph node metastasis patients (p=0.013). In LSCC patients, an increased expression of p62 was associated with poor cell differentiation (p=0.003) and p65-C expression was higher in older patients (>50 yrs, p=0.009). In OSCC patients, expression levels of LC3, p65-N, and p65-C were significantly different between three subsites (p<0.001). An increased expression of p62 (p=0.001) and p65-C p<0.001) was found in those with poor cell differentiation. The expressions of EGFR-C was accordingly associated in advanced AJCC pathological stage (p<0.001) and high T classification (p=0.006). An increased expression of p65-C (p=0.012) and EGFR-C (p=0.012) but a reduced expression of EGFR-M (p=0.019) were found in those with lymph node metastasis. Finally, the univariate and multivariate analysis of survival showed that a higher expression level of p62 was associated with a poor disease-specific survival (DSS) and disease-free survival (DFS) of OSCC patients, especially DSS for BMSCC patients) and DFS for LSCC. The LC3, p62, p65, and EGFR could be biomarkers for tumorigenesis in OSCC, including three primary subsites. Moreover, p62 is…
Advisors/Committee Members: Wen%20Shu%22%29&pagesize-30">
Chih-
Wen Shu (chair),
Ching-Mei Hsu (chair),
Jiin-Tsuey Cheng (committee member),
Luo-Ping Ger (committee member).
Subjects/Keywords: autophagy-related protein; immunohistochemistry; tumorigenesis; survival; Oral squamous cell carcinoma
Record Details
Similar Records
Cite
Share »
Record Details
Similar Records
Cite
« Share
❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Li, Y. (2016). LC3, P62, P65, and EGFR Protein Expressions are Associated with Tumor Transformation and Poor Prognosis in Oral Squamous Cell Carcinoma. (Thesis). NSYSU. Retrieved from http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0621116-000801
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):
Li, Yi-jing. “LC3, P62, P65, and EGFR Protein Expressions are Associated with Tumor Transformation and Poor Prognosis in Oral Squamous Cell Carcinoma.” 2016. Thesis, NSYSU. Accessed April 16, 2021.
http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0621116-000801.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Li, Yi-jing. “LC3, P62, P65, and EGFR Protein Expressions are Associated with Tumor Transformation and Poor Prognosis in Oral Squamous Cell Carcinoma.” 2016. Web. 16 Apr 2021.
Vancouver:
Li Y. LC3, P62, P65, and EGFR Protein Expressions are Associated with Tumor Transformation and Poor Prognosis in Oral Squamous Cell Carcinoma. [Internet] [Thesis]. NSYSU; 2016. [cited 2021 Apr 16].
Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0621116-000801.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Li Y. LC3, P62, P65, and EGFR Protein Expressions are Associated with Tumor Transformation and Poor Prognosis in Oral Squamous Cell Carcinoma. [Thesis]. NSYSU; 2016. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0621116-000801
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
NSYSU
3.
Mao, Pu-Wei.
Suppressive Effects of Probiotics on Salmonella Induced Inflammation.
Degree: Master, Biological Sciences, 2016, NSYSU
URL: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0729116-164844
► Salmonella infection in humans is commonly manifested as enterocolitis characterized by induction of epithelial secretion of pro-inflammatory cytokines and diarrhea, accompanied by infiltration of neutrophils…
(more)
▼ Salmonella infection in humans is commonly manifested as enterocolitis characterized by induction of epithelial secretion of pro-inflammatory cytokines and diarrhea, accompanied by infiltration of neutrophils in the intestinal submucosa, which is a hall-mark of intestinal inflammation. The recruitment of neutrophils from circulation to the subepithelial region is facilitated by chemokines such as interleukin-8 (IL-8), which is known to be significantly induced upon bacterial entry by host epithelial cells.
Probiotics are able to be used in the prevention or treatment of certain types of in-flammatory bowel disease (IBD). Certain types of Lactobacillus strains are successful in modulating pro-inflammatory cytokine signaling, which in turn, reduce inflammation in the gastrointestinal tract.
In this study, we used the human intestinal cell line HCT 116 as an intestinal epithelial model, and the human leukemic monocyte cell line THP-1 as a leukocyte model, to determine the effects of four arbitrarily chosen strains of Lactobacillus probiotics on inflammation caused by Salmonella infection. The Salmonella strain used in the study is the wild-type SL1344, grown under anaerobic conditions to late log phase to maximize invasion phenotype. The four probiotic strains are Lactobacillus acidophilus, Lactoba-cillus rhamnosus, Lactobacillus paracasei, and Lactobacillus delbrueckii.
Our results show that all four strains of probiotics were able to sporadically reduce mRNA expression of the three tested cytokines, but only Lactobacillus paracasei was able to consistently lower IL-8 expression. Our experimental results had shown in infection tests that upon Salmonella infection, the most acute response is seen in the upregu-lation of IL-8 expression, suggesting a possible relation between inflammation induced by bacterial infection and IL-8 induction. However, invasion assays show that Lactoba-cillus paracasei did not significantly reduce the amount of intracellular bacteria. In-stead, only Lactobacillus rhamnosus, which did not consistently suppress IL-8, signifi-cantly reduced bacterial invasion. These findings suggest that various probiotics sup-press inflammation through different mechanisms, and that the probiotic Lactobacillus rhamnosus is able to protect intestinal epithelial cells by rendering them less suscepti-ble to Salmonella invasion.
Advisors/Committee Members: I-Fei Huang (chair), Wen%20Shu%22%29&pagesize-30">
Chih-
Wen Shu (chair),
Chen Chun-Lin (committee member).
Subjects/Keywords: Salmonella; pro-inflammatory cytokine; inflammation; Lactobacillus; Probiotics; anti-inflammatory; intra-cellular pathogen
Record Details
Similar Records
Cite
Share »
Record Details
Similar Records
Cite
« Share
❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Mao, P. (2016). Suppressive Effects of Probiotics on Salmonella Induced Inflammation. (Thesis). NSYSU. Retrieved from http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0729116-164844
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):
Mao, Pu-Wei. “Suppressive Effects of Probiotics on Salmonella Induced Inflammation.” 2016. Thesis, NSYSU. Accessed April 16, 2021.
http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0729116-164844.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Mao, Pu-Wei. “Suppressive Effects of Probiotics on Salmonella Induced Inflammation.” 2016. Web. 16 Apr 2021.
Vancouver:
Mao P. Suppressive Effects of Probiotics on Salmonella Induced Inflammation. [Internet] [Thesis]. NSYSU; 2016. [cited 2021 Apr 16].
Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0729116-164844.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Mao P. Suppressive Effects of Probiotics on Salmonella Induced Inflammation. [Thesis]. NSYSU; 2016. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0729116-164844
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
NSYSU
4.
WU, HUI-CHUN.
Autophagy inducers modulated ATG4B expression in human brain tumor cells.
Degree: Master, Biological Sciences, 2018, NSYSU
URL: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0605118-111049
► Autophagy is a self-eating mechanism in cells through which damaged proteins and organelles are recruited to autophagosomes and fused with lysosome for their bulk degradation…
(more)
▼ Autophagy is a self-eating mechanism in cells through which damaged proteins and organelles are recruited to autophagosomes and fused with lysosome for their bulk degradation and recycling during nutrient deprivation. Dysregulation of autophagy is associated with various diseases, including cancer. ATG4B is a cysteine protease required for autophagy machinery. Recent reports have shown that elevated ATG4B promoted tumorigenesis, malignancy and drug resistance, suggesting ATG4B might modulate autophagy to facilitate tumor progression. However, the role of autophagy on ATG4B in cancer cells remains unknown. In this study, we found ATG4B protein level was decreased in glioma H4 and SHSY5Y cells during autophagy inducing conditions, including rapamycin and starvation. Moreover, autophagy inhibitors chloroquine or BafA1and proteosome inhibitor MG132 modestly recovered autophagy downregulated ATG4B in cells. Silencing ATG7 also partially recovered ATG4B protein level in cell treated with rapamycin, whereas it had no recovery effects in starved cells. Furthermore, mRNA level of ATG4B was decreased in rapamycin-treated H4 cells, but not starved cells. Luciferase fusion with 3âUTR of ATG4B as reporter assay was used to evaluate the effects of miRNA on ATG4B in cells during autophagy conditions. The luciferase activity was significantly decreased in H4 cells treated with rapamycin. However, the luciferase activity had little effects on recovery. The miR-34a was accordingly increased in the rapamycin-treated cells, while miR-34a was inhibited in BafA1 and CQ pretreated cells. Taken together, rapamycin may regulate autophagy and miR-34a to reduce ATG4B in glioma cells. Our results may shed a light on potential mechanisms of rapamycin on tumor suppression.
Advisors/Committee Members: Ming-Hong Tai (chair), Pei-Feng Liu (chair), Wen%20Shu%22%29&pagesize-30">
Chih-
Wen Shu (committee member),
Chen, Chun-Lin (committee member).
Subjects/Keywords: Rapamycin; Chloroquine; Glioma; Autophagy; ATG4B
Record Details
Similar Records
Cite
Share »
Record Details
Similar Records
Cite
« Share
❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
WU, H. (2018). Autophagy inducers modulated ATG4B expression in human brain tumor cells. (Thesis). NSYSU. Retrieved from http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0605118-111049
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, HUI-CHUN. “Autophagy inducers modulated ATG4B expression in human brain tumor cells.” 2018. Thesis, NSYSU. Accessed April 16, 2021.
http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0605118-111049.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
WU, HUI-CHUN. “Autophagy inducers modulated ATG4B expression in human brain tumor cells.” 2018. Web. 16 Apr 2021.
Vancouver:
WU H. Autophagy inducers modulated ATG4B expression in human brain tumor cells. [Internet] [Thesis]. NSYSU; 2018. [cited 2021 Apr 16].
Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0605118-111049.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
WU H. Autophagy inducers modulated ATG4B expression in human brain tumor cells. [Thesis]. NSYSU; 2018. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0605118-111049
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
NSYSU
5.
Chung, Chih-ling.
Study the effects of myosin V inhibitor, pentabromopseudilin , in TGF-β-induced responsiveness.
Degree: Master, Biological Sciences, 2018, NSYSU
URL: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0626118-141345
► Transforming Growth Factor-β (TGF-β) is a multifunctional cytokine that involved in many biological processes. TGF-β signaling transduction initiates when binding to Type II TGF-β receptor…
(more)
▼ Transforming Growth Factor-β (TGF-β) is a multifunctional cytokine that involved in many biological processes. TGF-β signaling transduction initiates when binding to Type II TGF-β receptor (TβRII). Once binding to TGF-β, TβRII forms heterocomplex with Type I TGF-β receptor (TβRI) and phosphorylates Smad2 and Smad3. P-Smad2/3 then forms a homotrimer with Smad4. Finally, R-Smad/Smad4 complexes are then translocated into the nucleus where they act as a transcriptional regulator of target genes. TGF-β signaling plays an opposite role during carcinoma progression. In the early stage, TGF-β acts as a tumor suppressor through inhibiting cell proliferation. Conversely, TGF-β promotes tumor cell proliferation and enhances mobility of cell in the late stage of carcinoma. In addition, TGF-β also is associated to other diseases such as organ fibrosis and autoimmune diseases. Pentabromopseudilin (PBrP) is a natural chlorinated phenylpyrrole compound that shows a broad range of antimicrobial activity. In mammalian cells, PBrP acts as an allosteric inhibitor of myosin 1c (Myo1c). In this study, we find that PBrP attenuates TGF-β responsiveness by promoting degradation of surface TβRII. Furthermore, PBrP inhibits TGF-β-induced Smad2/3 phosphorylation and plasminogen activator inhibitor-1 (PAI-1) promoter activation with a IC50 betewwn 0.05 μM to 0.1μM. Abolishing the process of epithelial-to-mesenchymal transition (EMT) in A549 and HepG2 cells, PBrP is found to suppress the mobility of cells. The results also demonstrate that PBrP directs surface TβR-II translocation to non-raft fractions from lipid raft. The translocation is followed by internalization and degradation of TβRII via lysosomal pathway. By accelerating TβR-II degradation, PBrP inhibits TGF-β-stimulated cellular responsiveness.
Advisors/Committee Members: Tsong-Long Hwang (chair), Ping-Jyun Sung (chair), Chun-Lin Chen (committee member), Wen%20Shu%22%29&pagesize-30">
Chih-
Wen Shu (chair).
Subjects/Keywords: Myosin Va; lipid raft; small molecular inhibitors; Pentabromopseudilin; TGF-β
Record Details
Similar Records
Cite
Share »
Record Details
Similar Records
Cite
« Share
❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Chung, C. (2018). Study the effects of myosin V inhibitor, pentabromopseudilin , in TGF-β-induced responsiveness. (Thesis). NSYSU. Retrieved from http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0626118-141345
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):
Chung, Chih-ling. “Study the effects of myosin V inhibitor, pentabromopseudilin , in TGF-β-induced responsiveness.” 2018. Thesis, NSYSU. Accessed April 16, 2021.
http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0626118-141345.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Chung, Chih-ling. “Study the effects of myosin V inhibitor, pentabromopseudilin , in TGF-β-induced responsiveness.” 2018. Web. 16 Apr 2021.
Vancouver:
Chung C. Study the effects of myosin V inhibitor, pentabromopseudilin , in TGF-β-induced responsiveness. [Internet] [Thesis]. NSYSU; 2018. [cited 2021 Apr 16].
Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0626118-141345.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Chung C. Study the effects of myosin V inhibitor, pentabromopseudilin , in TGF-β-induced responsiveness. [Thesis]. NSYSU; 2018. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0626118-141345
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
NSYSU
6.
Wang, Shi-Wei.
Study the effects of sorafenib in TGF-β signaling.
Degree: Master, Biological Sciences, 2018, NSYSU
URL: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0627118-110916
► The multi-kinase inhibitor sorafenib is the FDA approved drug for the treatment of advanced hepatocellular carcinoma (HCC) and other solid tumors. Previous studies have showed…
(more)
▼ The multi-kinase inhibitor sorafenib is the FDA approved drug for the treatment of advanced hepatocellular carcinoma (HCC) and other solid tumors. Previous studies have showed that Transforming Growth Factor-β (TGF-β) signaling may help tumor progression in HCC. Both autocrine and paracrine TGF-β promote tumor growth, enhance metastasis ability and malignancy by inducing epithelial -mesenchymal transition (EMT). Sorafenib is thought to suppress tumor progression by inhibiting TGF-β induced EMT and tissue fibrosis. However HCC is resistant to sorafenib in patients and causes relapse, of which the detailed mechanism remains unknown. In this study, we found that sorafenib specific decreased cell surface TGF-β type II receptor in HCCs and hepatocytes (Hep-G2, Clone9) by increasing TβRII internalization through lipid-raft/caveolae-mediate endocytosis and then degrade in lysosome. Sorafenib-induced downregulation and degradation of TβRII can be protected by caveolae and lysosome inhibitor. On the other hands, sorafenib just affected TβRII localization in lipid-raft/caveolae but not in non-lipid raft on hepatic stellate cells (HSCs) so that TGF-β still induced smad2/3 signaling pathway in HSCs . Our result showed that sorafenib mainly induced TβRII internalization through lipid-raft/caveolae-mediate endocytosis and caused degradation of TGF-β type II receptor for suppression of TGF-β signaling. By gathering TβRII in lipid-raft or using TGF-β receptor kinase inhibitor may provide a direction of sorafenib treat with HCC and TGF-β related diseases.
Advisors/Committee Members: Tsong-Long Hwang (chair), Chun-Lin Chen (committee member), Ping-Jyun Sung (chair), Wen%20Shu%22%29&pagesize-30">
Chih-
Wen Shu (chair).
Subjects/Keywords: Lipid-raft/caveolae; hepatocellular carcinoma; Sorafenib; TGF-β; Endocytosis/degradation
Record Details
Similar Records
Cite
Share »
Record Details
Similar Records
Cite
« Share
❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Wang, S. (2018). Study the effects of sorafenib in TGF-β signaling. (Thesis). NSYSU. Retrieved from http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0627118-110916
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):
Wang, Shi-Wei. “Study the effects of sorafenib in TGF-β signaling.” 2018. Thesis, NSYSU. Accessed April 16, 2021.
http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0627118-110916.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Wang, Shi-Wei. “Study the effects of sorafenib in TGF-β signaling.” 2018. Web. 16 Apr 2021.
Vancouver:
Wang S. Study the effects of sorafenib in TGF-β signaling. [Internet] [Thesis]. NSYSU; 2018. [cited 2021 Apr 16].
Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0627118-110916.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Wang S. Study the effects of sorafenib in TGF-β signaling. [Thesis]. NSYSU; 2018. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0627118-110916
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
NSYSU
7.
Yang, Hsiu-Chen.
The Role of ESCRT-1 member Tumor Susceptibility Gene 101 in Cellular Autophagic Pathway.
Degree: Master, Biological Sciences, 2014, NSYSU
URL: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0721114-182635
► The endocytosis involves in a variety of cellular activities including nutrient intake, and receptor recycling or degradation. The endosomal sorting complexes required for transport (ESCRTs)…
(more)
▼ The endocytosis involves in a variety of cellular activities including nutrient intake, and receptor recycling or degradation. The endosomal sorting complexes required for transport (ESCRTs) plays an important role that orchestrate the formation of multivesicular bodies (MVBs), which regulates protein sorting and vesicular trafficking. Tumor Susceptibility Gene 101(TSG101) is a member of ESCRT-I responsible for sorting ubiquitin-modified protein into MVBs. The endocytic and autophagic pathways merge at the lysosomal compartment. Proteins sorting into the MVBs are processed upon fusion of autophagosome and lysosome to form autophagolysosome by lysosomal enzymatic digestion. The autophagosome can fuse with endosomes/multivesicular bodies to generate the amphisome for degradation cargo containing both autophagic and endocytic materials. This autophagic pathway plays a critical role for cellular physiological homeostasis by clearing misfolded protein, aberrant accumulation of ubiquitin modified proteins, and damaged organelles. Recent reports confirmed that abnormal endocytic pathway may affect autophagic process, which is critical for the prevention of cancer or neuronal degenerative diseases. In addition, SQSTM1/p62 contains an ubiquitin binding domain that can bind to the ubiquitylated proteins destined for selective degradation. The accumulation of SQSTM1/p62 serves as a marker for perturbation of autophagic process. Our previous data indicated that TSG101 and MAP1LC3-II are upregulated simultaneously upon starvation or autophagic induction with rapamycin. In this study, the neuroblastoma SH-SY5Y and GFP-LC3 autophagic reporter cell lines were used to investigate the effect of TSG101 on the LC3-II, p62 and ubiquitinated protein levels upon deprivation of TSG101 using siRNA in conjunction with the treatment of autophagic modulators, rapamycin and chloroquine. We found that silencing of TSG101 resulted in the accumulation of MAP1LC3-II, SQSTM1/p62, and ubiqutinated proteins. The number of GFP-LC3 puncta was increased in TSG101 knockdown SHSY5Y cells, while co-localization of DsRed-Rab7-associated MVB and autophagosome were diminished, suggesting TSG101 may facilitate fusion steps of autophagosome with MVB to promote autophagic activity. These results provide the new role and molecular mechanism of TSG101 in the autophagic pathway.
Advisors/Committee Members: Jiin-Tsuey Cheng (committee member), Lu-Shiun Her (chair), Wen%20Shu%22%29&pagesize-30">
Chih-
Wen Shu (committee member),
Guang-Chao Chen (chair),
Yi-Ren Hong (chair).
Subjects/Keywords: MAP1LC3-II; Autophagy; amphisome; rapamycin; ESCRT; Tumor Susceptibility Gene 101
Record Details
Similar Records
Cite
Share »
Record Details
Similar Records
Cite
« Share
❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Yang, H. (2014). The Role of ESCRT-1 member Tumor Susceptibility Gene 101 in Cellular Autophagic Pathway. (Thesis). NSYSU. Retrieved from http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0721114-182635
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, Hsiu-Chen. “The Role of ESCRT-1 member Tumor Susceptibility Gene 101 in Cellular Autophagic Pathway.” 2014. Thesis, NSYSU. Accessed April 16, 2021.
http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0721114-182635.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Yang, Hsiu-Chen. “The Role of ESCRT-1 member Tumor Susceptibility Gene 101 in Cellular Autophagic Pathway.” 2014. Web. 16 Apr 2021.
Vancouver:
Yang H. The Role of ESCRT-1 member Tumor Susceptibility Gene 101 in Cellular Autophagic Pathway. [Internet] [Thesis]. NSYSU; 2014. [cited 2021 Apr 16].
Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0721114-182635.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Yang H. The Role of ESCRT-1 member Tumor Susceptibility Gene 101 in Cellular Autophagic Pathway. [Thesis]. NSYSU; 2014. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0721114-182635
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
. 
Open Access Theses and Dissertations