Abstract
Nonsteroidal antiinflammatory drugs (NSAIDs) can inhibit colorectal tumorigenesis and are among the few agents known to be useful for the chemoprevention of neoplasia. Here, we show that the tumor suppressive effects of NSAIDs are not likely to be related to a reduction in prostaglandins but rather are due to the elevation of the prostaglandin precursor arachidonic acid (AA). NSAID treatment of colon tumor cells results in a dramatic increase in AA that in turn stimulates the conversion of sphingomyelin to ceramide, a known mediator of apoptosis. These results have significant implications for understanding and improving colon cancer chemoprevention.
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Dates
Type | When |
---|---|
Created | 23 years, 1 month ago (July 26, 2002, 10:40 a.m.) |
Deposited | 2 years, 4 months ago (April 22, 2023, 8:26 a.m.) |
Indexed | 1 week, 3 days ago (Aug. 26, 2025, 2:24 a.m.) |
Issued | 27 years, 7 months ago (Jan. 20, 1998) |
Published | 27 years, 7 months ago (Jan. 20, 1998) |
Published Online | 27 years, 7 months ago (Jan. 20, 1998) |
Published Print | 27 years, 7 months ago (Jan. 20, 1998) |
@article{Chan_1998, title={Mechanisms underlying nonsteroidal antiinflammatory drug-mediated apoptosis}, volume={95}, ISSN={1091-6490}, url={http://dx.doi.org/10.1073/pnas.95.2.681}, DOI={10.1073/pnas.95.2.681}, number={2}, journal={Proceedings of the National Academy of Sciences}, publisher={Proceedings of the National Academy of Sciences}, author={Chan, Timothy A. and Morin, Patrice J. and Vogelstein, Bert and Kinzler, Kenneth W.}, year={1998}, month=jan, pages={681–686} }