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, 22 August 2006
Vol. 2006, Issue 349, p. tw287
[DOI: 10.1126/stke.3492006tw287]

EDITORS' CHOICE

CANCER p53 and Tumor Angiogenesis

The tumor suppressor protein p53 transcriptionally activates genes that control cell cycle arrest, apoptosis, and other cellular processes that help to prevent tumor development. Teodoro et al. now show that p53 appears to keep tumors in check by activating the gene encoding α(II) collagen prolyl-4-hydroxylase. This enzyme is required for the extracellular release of collagen-derived peptides, such as endostatin and tumstatin, that are potent inhibitors of tumor angiogenesis. The p53 gene is inactivated in many human cancers, presumably leading to reduced production of endogenous antiangiogenic peptides that defend against tumor growth.

J. G. Teodoro, A. E. Parker, X. Zhu, M. R. Green, p53-Mediated inhibition of angiogenesis through up-regulation of a collagen prolyl hydroxylase. Science 313, 968-971 (2006). [Abstract] [Full Text]

Citation: p53 and Tumor Angiogenesis. Sci. STKE 2006, tw287 (2006).


To Advertise     Find Products


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