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The role of p38 mitogen activated pr...
~
Khatri, Jitender.
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The role of p38 mitogen activated protein kinase in post-transcriptional regulation of cyclooxygenase-2 in intleukin-1beta and tumor necrosis factor-alpha stimulated prostate cancer cell lines.
Record Type:
Language materials, printed : Monograph/item
Title/Author:
The role of p38 mitogen activated protein kinase in post-transcriptional regulation of cyclooxygenase-2 in intleukin-1beta and tumor necrosis factor-alpha stimulated prostate cancer cell lines./
Author:
Khatri, Jitender.
Description:
67 p.
Notes:
Source: Dissertation Abstracts International, Volume: 72-08, Section: B, page: .
Contained By:
Dissertation Abstracts International72-08B.
Subject:
Biology, Molecular. -
Online resource:
http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3459190
ISBN:
9781124693804
The role of p38 mitogen activated protein kinase in post-transcriptional regulation of cyclooxygenase-2 in intleukin-1beta and tumor necrosis factor-alpha stimulated prostate cancer cell lines.
Khatri, Jitender.
The role of p38 mitogen activated protein kinase in post-transcriptional regulation of cyclooxygenase-2 in intleukin-1beta and tumor necrosis factor-alpha stimulated prostate cancer cell lines.
- 67 p.
Source: Dissertation Abstracts International, Volume: 72-08, Section: B, page: .
Thesis (Ph.D.)--University of Massachusetts Lowell, 2011.
Cyclooxygenase (COX) the rate-limiting enzyme in prostaglandin (PG) synthesis exists in two principle isoforms, COX-1 and COX-2. A considerable body of evidence implicates COX-2 (and hence PG) up-regulation as a major factor in carcinogenesis in many tissues. In previous work, we have determined that the half-life of COX-2 mRNA is significantly increased in cytokine-stimulated human and rat cells. The objective of this work was to determine the putative molecular mechanisms that operate in human COX-2 mRNA stabilization by p38 mitogen activated protein kinase (MAPK) in normal and prostate cancer cell lines. I show that COX-2 up-regulation in human prostate cancer cells is, in part, induced by the stabilization of the COX-2 mRNA transcript by p38 MAPK.
ISBN: 9781124693804Subjects--Topical Terms:
1017719
Biology, Molecular.
The role of p38 mitogen activated protein kinase in post-transcriptional regulation of cyclooxygenase-2 in intleukin-1beta and tumor necrosis factor-alpha stimulated prostate cancer cell lines.
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The role of p38 mitogen activated protein kinase in post-transcriptional regulation of cyclooxygenase-2 in intleukin-1beta and tumor necrosis factor-alpha stimulated prostate cancer cell lines.
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Source: Dissertation Abstracts International, Volume: 72-08, Section: B, page: .
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Adviser: Bruce Jackson.
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Thesis (Ph.D.)--University of Massachusetts Lowell, 2011.
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Cyclooxygenase (COX) the rate-limiting enzyme in prostaglandin (PG) synthesis exists in two principle isoforms, COX-1 and COX-2. A considerable body of evidence implicates COX-2 (and hence PG) up-regulation as a major factor in carcinogenesis in many tissues. In previous work, we have determined that the half-life of COX-2 mRNA is significantly increased in cytokine-stimulated human and rat cells. The objective of this work was to determine the putative molecular mechanisms that operate in human COX-2 mRNA stabilization by p38 mitogen activated protein kinase (MAPK) in normal and prostate cancer cell lines. I show that COX-2 up-regulation in human prostate cancer cells is, in part, induced by the stabilization of the COX-2 mRNA transcript by p38 MAPK.
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The human prostate cancer cell lines DU145 and PC3 were utilized in this study. I have determined that MAPK inhibitors down-regulate COX-2 mRNA levels in stimulated DU145 and PC-3 human prostate cancer cells but not in the normal prostate cell line, CRL2221. I found that DU145 cells treated with the specific p38 MAPK inhibitor, SB203580, showed significant decreases in COX-2 mRNA levels relative to the identically treated CRL2221 cells. In the present study, I also provide evidence that p38 MAPK pathway regulates stability of COX-2 mRNA and hence PG production in DU145 and PC3 cells. This inhibitory effect, however, is significantly less in CRL221 cells.
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http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3459190
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