Journal
CANCER CELL
Volume 6, Issue 3, Pages 285-295Publisher
CELL PRESS
DOI: 10.1016/j.ccr.2004.08.011
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Funding
- NCI NIH HHS [P0 CA 77839] Funding Source: Medline
- NICHD NIH HHS [HD 33994, R37 HD 12304] Funding Source: Medline
- NIDA NIH HHS [DA 06668] Funding Source: Medline
- NIDDK NIH HHS [R01 DK 47279, R37 DK 47297] Funding Source: Medline
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Cyclooxygenase-derived prostaglandin E-2 (PGE(2)) is the predominant prostanoid found in most colorectal cancers (CRC) and is known to promote colon carcinoma growth and invasion. However, the key downstream signaling pathways necessary for PGE(2)-induced intestinal carcinogenesis are unclear. Here we report that PGE(2) indirectly transactivates PPARdelta through PI3K/Akt signaling, which promotes cell survival and intestinal adenoma formation. We also found that PGE2 treatment of Apc(min) mice dramatically increased intestinal adenoma burden, which was negated in Apc(min) mice lacking PPARdelta. We demonstrate that PPARdelta is a focal point of crosstalk between the prostaglandin and Wnt signaling pathways which results in a shift from cell death to cell survival, leading to increased tumor growth.
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