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You searched for subject:(prostasin). Showing records 1 – 3 of 3 total matches.

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NSYSU

1. Lin, Chun-kuang. Development of antiviral drugs from marine natural products and investigation of drug target against virus.

Degree: PhD, Doctoral Degree Program in Marine Biotechnology, 2018, NSYSU

Hepatitis C virus (HCV) infection causes chronic inflammation of liver, leading to the development of cirrhosis and hepatocellular carcinoma (HCC). Infection of dengue virus (DENV) caused diseases ranging from acute self-limiting febrile illness to life-threatening dengue hemorrhagic fever and dengue shock syndrome. The purposes of present dissertation are to discover the anti-viral agents from marine natural products and to investigate the impact of cellular factors on DENV replication. For finding the potential antivirals, we found that betulinic acid (BA) and acteoside (AM-4) extracted from Avicennia marina could reduce HCV replication. The mechanism study demonstrated that BA reduced HCV replication through decreasing the NF-κB- and ERK1/2-mediated cyclooxygenase-2 (COX-2) expression. The AM-4 suppressed HCV infection by blocking viral entry into cells and cell-to-cell spread of HCV. In addition, we identified that lobohedleolide extracted from soft coral exhibited anti-HCV activity by suppression of HCV-induced COX-2 expression. Using various COX-2 promoter deletion constructs linked to luciferase reporter gene, we first identified CCAAT/enhancer-binding protein (C/EBP) as a key transcription factor for the down-regulation of COX-2 by lobohedleolide, and then demonstrated that the HCV-induced C/EBP expression could be suppressed by lobohedleolide through inhibiting the phosphorylation of JNK and c-Jun. Notably, combination treatment of BA, AM-4 and lobohedleolide with several clinically used HCV drugs synergistically inhibited HCV RNA replication, indicating that these three natural products exhibited a high biomedical potential to be used as a supplementary agent for control of HCV infection. Besides, BA and lobohedleolide also exhibited anti-DENV activity. For finding the therapeutic targets from cellular gene against DENV, we observed an increased level of COX-2 in patients with dengue fever compared with healthy individuals. Then, an elevated level of COX-2 expression was also observed in DENV-infected ICR suckling mice. COX-2 gene silencing and catalytic inhibition sufficiently suppressed DENV-2 replication. Using ICR suckling mouse model, we identified that the COX-2 inhibitor NS398 protected mice from succumbing to life-threatening DENV-2 infection, revealing targeting COX-2 is a promising strategy to control DENV infection. In addition, we found that the expression of prostasin, a serine protease, is lower in patients with dengue fever than in healthy individuals. Exogenous expression of prostasin could protect ICR suckling mice from life-threatening DENV-2 infection and reduce DENV-2 propagation in Huh-7 cells. We further revealed that prostasin reduced DENV replication through proteolytic cleavage of epithelial growth factor receptor (EGFR). The activity of proteolytic cleavage of prostasin is dependent on the expression of matriptase and hepatocyte growth factor activator inhibitor type 2 (HAI-2). Collectively, COX-2 and prostasin exhibited highly potential to serve as therapeutic targets against… Advisors/Committee Members: Jyh-Horng Sheu (chair), Jin-Ching Lee (chair), Shih-Hsiung Wu (chair), Chih-Chuang Liaw (committee member), Yen-Hsu Chen (chair).

Subjects/Keywords: DENV; COX-2; marine natural product; EGFR; prostasin; HCV

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APA (6th Edition):

Lin, C. (2018). Development of antiviral drugs from marine natural products and investigation of drug target against virus. (Doctoral Dissertation). NSYSU. Retrieved from http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0019118-192352

Chicago Manual of Style (16th Edition):

Lin, Chun-kuang. “Development of antiviral drugs from marine natural products and investigation of drug target against virus.” 2018. Doctoral Dissertation, NSYSU. Accessed November 23, 2020. http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0019118-192352.

MLA Handbook (7th Edition):

Lin, Chun-kuang. “Development of antiviral drugs from marine natural products and investigation of drug target against virus.” 2018. Web. 23 Nov 2020.

Vancouver:

Lin C. Development of antiviral drugs from marine natural products and investigation of drug target against virus. [Internet] [Doctoral dissertation]. NSYSU; 2018. [cited 2020 Nov 23]. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0019118-192352.

Council of Science Editors:

Lin C. Development of antiviral drugs from marine natural products and investigation of drug target against virus. [Doctoral Dissertation]. NSYSU; 2018. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0019118-192352


University of Central Florida

2. Chen, Mengqian. Mechanism Of Action And Regulation Of Membrane Serine Protease Prostasin In The Prostate And Prostate Cancer.

Degree: 2007, University of Central Florida

The glycosylphosphatidylinositol (GPI)-anchored serine protease prostasin (PRSS8) is expressed at the apical membrane surface of epithelial cells and acts as a suppressor of tumor invasion when re-expressed in highly invasive human prostate and breast cancer cell lines. To better understand the molecular mechanisms underlying the anti-invasion phenotype associated with prostasin re-expression in prostate cancer cells, we expressed wild-type human prostasin or a serine active-site mutant prostasin in the PC-3 human prostate carcinoma cells. Molecular changes were measured at the mRNA and the protein levels. The expression of several invasion-promoting molecules is regulated by prostasin re-expression, mediated by a protein-level down-regulation of the epidermal growth factor receptor (EGFR). As a result, the cellular response to EGF was reduced as shown by the down-regulation of EGF-stimulated Erk1/2 phosphorylation. The expression of Slug, urokinase-type plasminogen activator (uPA), urokinase-type plasminogen activator receptor (uPAR), inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), and granulocyte-macrophage colony stimulating factor (GM-CSF) was also down-regulated by prostasin re-expression in the PC-3 cells. Co-expression of prostasin and its activating protease matriptase with EGFR in FT-293 cells induces an apparent proteolytic cleavage of the EGFR in the extracellular domain at two specific sites, generating two N-terminally truncated EGFR fragments, named EGFR135 and EGFR110. The EGFR110 is constitutively tyrosine-phosphorylated, and in its presence the phosphorylation of downstream signaling molecules including Erk1/2 and Akt is increased under serum-free conditions. Neither EGFR135 nor EGFR110 is responsive to EGF stimulation. Deletions of the EGFR extracellular domain (ECD) were generated to map the matriptase-prostasin cleavage sites. Two candidate sites were localized to regions AA1-273 and AA273-410. These data support a mechanism of action for the matriptase-prostasin epithelial extracellular serine protease activation cascade by proteolytically modulating the EGF-EGFR signaling. Prostasin gene expression is down-regulated in high-grade and hormone-refractory prostate cancers. We investigated the mechanisms by which androgens regulate prostasin expression in the prostate and prostate cancer. We treated the LNCaP human prostate cancer cells with dihydrotestosterone (DHT) and measured the mRNA expression of prostasin and potential transcription regulators of prostasin predicted by interrogation of the prostasin gene promoter sequence. Prostasin mRNA expression in the LNCaP cells was not responsive to DHT treatment. DHT marginally up-regulated mRNA expression of SREBP-1c, SREBP-2, and SNAIL, but not SREBP-1a, while dramatically increased SLUG mRNA expression, in a dose-dependent manner. Co-transfection of a prostasin promoter-reporter and SREBP cDNA in HEK-293 cells resulted in stimulation of the promoter activity at ~2 fold by SREBP-1c, and up to 6 fold by SREBP-2; while co-transfection… Advisors/Committee Members: Chai, Karl.

Subjects/Keywords: Prostasin; EGFR; prostate cancer; SREBP; Slug; Matriptase; Cancer Biology; Microbiology; Molecular Biology

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APA (6th Edition):

Chen, M. (2007). Mechanism Of Action And Regulation Of Membrane Serine Protease Prostasin In The Prostate And Prostate Cancer. (Doctoral Dissertation). University of Central Florida. Retrieved from https://stars.library.ucf.edu/etd/3115

Chicago Manual of Style (16th Edition):

Chen, Mengqian. “Mechanism Of Action And Regulation Of Membrane Serine Protease Prostasin In The Prostate And Prostate Cancer.” 2007. Doctoral Dissertation, University of Central Florida. Accessed November 23, 2020. https://stars.library.ucf.edu/etd/3115.

MLA Handbook (7th Edition):

Chen, Mengqian. “Mechanism Of Action And Regulation Of Membrane Serine Protease Prostasin In The Prostate And Prostate Cancer.” 2007. Web. 23 Nov 2020.

Vancouver:

Chen M. Mechanism Of Action And Regulation Of Membrane Serine Protease Prostasin In The Prostate And Prostate Cancer. [Internet] [Doctoral dissertation]. University of Central Florida; 2007. [cited 2020 Nov 23]. Available from: https://stars.library.ucf.edu/etd/3115.

Council of Science Editors:

Chen M. Mechanism Of Action And Regulation Of Membrane Serine Protease Prostasin In The Prostate And Prostate Cancer. [Doctoral Dissertation]. University of Central Florida; 2007. Available from: https://stars.library.ucf.edu/etd/3115


University of Central Florida

3. Hatfield, Meghan. Prostasin Is Expressed In Benign Prostatic Hyperplasia And Regulates Cell Proliferation And Invasion Via Inos, Icam-1, And Cycli.

Degree: 2008, University of Central Florida

Prostasin is expressed in normal prostate epithelial cells but down-regulated in prostate cancers, while prostasin re-expression in invasive prostate cancer cells reduced invasion. We examined prostasin expression and function in benign prostatic hyperplasia (BPH). We evaluated prostasin expression in 12 BPH specimens by immunohistochemistry, and evaluated the impact of prostasin silencing by siRNA on the expression of the inducible nitric oxide synthase (iNOS), intercellular adhesion molecule-1 (ICAM-1), and cyclin D1, as well as on cell proliferation and invasion, using the BPH-1 human prostate epithelial cell line model. Prostasin expression was localized in the glands of BPH tissues by immunohistochemistry, in either the tall columnar-shaped or the flattened epithelial cells. We silenced prostasin expression by >50% at both the mRNA and protein levels using siRNA in the BPH-1 human prostate epithelial cell line, and this silencing of prostasin expression was associated with an induction of iNOS and ICAM-1 expression and a down-regulation of cyclin D1 expression. The protein expression of EGFR, a putative prostasin substrate, was not affected by prostasin silencing in this cell line. The prostasin-silenced cells displayed a reduced cell proliferation rate and reduced invasiveness, cell behaviors regulated by cyclin D1, iNOS, and ICAM-1 in the BPH-1 cells. We believe that this down-regulation of cyclin D1 is due to prostasin's augmentative effect on iNOS. We also believe that the decrease in cell motility is due to an increase in iNOS and ICAM-1 as well as a decrease in cyclin D1, since all of these molecules can play a role in cell motility. In conclusion, Prostasin is somehow involved in the regulation of inflammatory gene expression (iNOS and ICAM-1) in prostate epithelial cells, as well as cyclin D1 expression, cell proliferation and invasion, involving molecular mechanisms different than those in the prostate cancer cells. These studies suggest that prostasin is a player in the glandular components of benign prostatic hyperplasia. Advisors/Committee Members: Chai, Karl.

Subjects/Keywords: Prostasin; GPI-anchor; BPH; Invasion; Cancer Biology; Microbiology; Molecular Biology

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6th Edition):

Hatfield, M. (2008). Prostasin Is Expressed In Benign Prostatic Hyperplasia And Regulates Cell Proliferation And Invasion Via Inos, Icam-1, And Cycli. (Masters Thesis). University of Central Florida. Retrieved from https://stars.library.ucf.edu/etd/3713

Chicago Manual of Style (16th Edition):

Hatfield, Meghan. “Prostasin Is Expressed In Benign Prostatic Hyperplasia And Regulates Cell Proliferation And Invasion Via Inos, Icam-1, And Cycli.” 2008. Masters Thesis, University of Central Florida. Accessed November 23, 2020. https://stars.library.ucf.edu/etd/3713.

MLA Handbook (7th Edition):

Hatfield, Meghan. “Prostasin Is Expressed In Benign Prostatic Hyperplasia And Regulates Cell Proliferation And Invasion Via Inos, Icam-1, And Cycli.” 2008. Web. 23 Nov 2020.

Vancouver:

Hatfield M. Prostasin Is Expressed In Benign Prostatic Hyperplasia And Regulates Cell Proliferation And Invasion Via Inos, Icam-1, And Cycli. [Internet] [Masters thesis]. University of Central Florida; 2008. [cited 2020 Nov 23]. Available from: https://stars.library.ucf.edu/etd/3713.

Council of Science Editors:

Hatfield M. Prostasin Is Expressed In Benign Prostatic Hyperplasia And Regulates Cell Proliferation And Invasion Via Inos, Icam-1, And Cycli. [Masters Thesis]. University of Central Florida; 2008. Available from: https://stars.library.ucf.edu/etd/3713

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