Note to users. If you're seeing this message, it means that your browser cannot find this page's style/presentation instructions -- or possibly that you are using a browser that does not support current Web standards. Find out more about why this message is appearing, and what you can do to make your experience of our site the best it can be.

Sci. STKE, 6 December 2005
Vol. 2005, Issue 313, p. tw433
[DOI: 10.1126/stke.3132005tw433]


CANCER Colon Cancer Connections

A previously unrecognized connection between two well-known signaling pathways appears to provide a crucial mechanism for control of proliferation of colon cancer cells. Castellone et al. show that the EP2 subtype of prostaglandin E2 receptor mounts a two-pronged attack that activates a transcriptional program that favors cell proliferation. When PGE2 binds to EP2, the associated heterotrimeric guanine nucleotide-binding protein (G protein) is activated. The G protein β{gamma} and α subunits act through distinct pathways that converge to promote stabilization and nuclear translocation of β-catenin, a protein that promotes transcription of specific genes that increase proliferation of cancer cells. This signaling system may explain why nonsteroidal anti-inflammatory drugs, which inhibit signaling through PGE2, can at times inhibit development of colon cancer in mice and human patients.

M. D. Castellone, H. Teramoto, B. O. Williams, K. M. Druey, J. S. Gutkind, Prostaglandin E2 promotes colon cancer cell growth through a Gs-axin-β-catenin signaling axis. Science 310, 1504-1510 (2005). [Abstract] [Full Text]

Citation: Colon Cancer Connections. Sci. STKE 2005, tw433 (2005).

To Advertise     Find Products

Science Signaling. ISSN 1937-9145 (online), 1945-0877 (print). Pre-2008: Science's STKE. ISSN 1525-8882