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Green tea constituent epigallocatechin‐3‐gallate selectively inhibits COX‐2 without affecting COX‐1 expression in human prostate carcinoma cells
Overexpression of cyclooxygenase (COX)‐2 has been implicated in many pathologic conditions, including cancer. One practical inference of this finding is that sustained inhibition of COX‐2 could serve as a promising target for prevention or therapy of cancer. Conventional nonsteroidal antiinflammator...
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Published in: | International journal of cancer 2005-02, Vol.113 (4), p.660-669 |
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Main Authors: | , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | Overexpression of cyclooxygenase (COX)‐2 has been implicated in many pathologic conditions, including cancer. One practical inference of this finding is that sustained inhibition of COX‐2 could serve as a promising target for prevention or therapy of cancer. Conventional nonsteroidal antiinflammatory drugs (NSAIDs) and recently developed COX‐2‐specific inhibitors have shown considerable promise in prevention of some forms of human cancer; however, its application is limited due to severe toxic side effects on normal cells. Therefore, there is a need to define novel, nontoxic dietary constituents with proven chemopreventive effects through other pathways that also possess COX‐2 but not COX‐1 inhibitory activity. Recent studies on green tea and its major polyphenolic constituent (‐)epigallocatechin‐3‐gallate (EGCG) have established its remarkable cancer preventive and some cancer therapeutic effects. Here, we show that EGCG inhibits COX‐2 without affecting COX‐1 expression at both the mRNA and protein levels, in androgen‐sensitive LNCaP and androgen‐insensitive PC‐3 human prostate carcinoma cells. Based on our study, it is tempting to suggest that a combination of EGCG with chemotherapeutic drugs could be an improved strategy for prevention and treatment of prostate cancer. |
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ISSN: | 0020-7136 1097-0215 |
DOI: | 10.1002/ijc.20629 |