Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2004-12-7
pubmed:abstractText
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.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
http://linkedlifedata.com/resource/pubmed/chemical/Antineoplastic Agents, http://linkedlifedata.com/resource/pubmed/chemical/Arachidonic Acid, http://linkedlifedata.com/resource/pubmed/chemical/Catechin, http://linkedlifedata.com/resource/pubmed/chemical/Cyclooxygenase 1, http://linkedlifedata.com/resource/pubmed/chemical/Cyclooxygenase 2, http://linkedlifedata.com/resource/pubmed/chemical/Dinoprostone, http://linkedlifedata.com/resource/pubmed/chemical/Isoenzymes, http://linkedlifedata.com/resource/pubmed/chemical/Membrane Proteins, http://linkedlifedata.com/resource/pubmed/chemical/PTGS1 protein, human, http://linkedlifedata.com/resource/pubmed/chemical/PTGS2 protein, human, http://linkedlifedata.com/resource/pubmed/chemical/Prostaglandin-Endoperoxide Synthases, http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger, http://linkedlifedata.com/resource/pubmed/chemical/Tea, http://linkedlifedata.com/resource/pubmed/chemical/Urokinase-Type Plasminogen Activator, http://linkedlifedata.com/resource/pubmed/chemical/epigallocatechin gallate
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0020-7136
pubmed:author
pubmed:issnType
Print
pubmed:day
10
pubmed:volume
113
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
660-9
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed-meshheading:15455372-Antineoplastic Agents, pubmed-meshheading:15455372-Apoptosis, pubmed-meshheading:15455372-Arachidonic Acid, pubmed-meshheading:15455372-Catechin, pubmed-meshheading:15455372-Cell Division, pubmed-meshheading:15455372-Cyclooxygenase 1, pubmed-meshheading:15455372-Cyclooxygenase 2, pubmed-meshheading:15455372-Dinoprostone, pubmed-meshheading:15455372-Humans, pubmed-meshheading:15455372-Isoenzymes, pubmed-meshheading:15455372-Male, pubmed-meshheading:15455372-Membrane Proteins, pubmed-meshheading:15455372-Prostaglandin-Endoperoxide Synthases, pubmed-meshheading:15455372-Prostatic Neoplasms, pubmed-meshheading:15455372-RNA, Messenger, pubmed-meshheading:15455372-Reverse Transcriptase Polymerase Chain Reaction, pubmed-meshheading:15455372-Tea, pubmed-meshheading:15455372-Tumor Cells, Cultured, pubmed-meshheading:15455372-Urokinase-Type Plasminogen Activator
pubmed:year
2005
pubmed:articleTitle
Green tea constituent epigallocatechin-3-gallate selectively inhibits COX-2 without affecting COX-1 expression in human prostate carcinoma cells.
pubmed:affiliation
University of Wisconsin, Department of Dermatology, 1300 University Ave., Madison, WI 53706, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, U.S. Gov't, Non-P.H.S., Research Support, Non-U.S. Gov't