Journal
FEBS LETTERS
Volume 579, Issue 17, Pages 3497-3502Publisher
WILEY
DOI: 10.1016/j.febslet.2005.05.030
Keywords
Csk; colon cancer; Src; colonic hyperproliferation
Funding
- NCI NIH HHS [1U01CA11125-01] Funding Source: Medline
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Hyperproliferation of the premalignant epithelium is critical for colonic carcinogenesis; however the mechanisms remain largely unexplored. We report herein that prior to occurrence of neoplastic lesions in the azoxymethane-rat model of colon carcinogenesis; the tumor suppressor gene C-terminal Src kinase (Csk) was down-regulated with a concomitant increase in Src activity. Furthermore, pharmacological or genetic (RNA interference) inhibition of Csk resulted in increased proliferation in colon cancer cell lines through the mitogen-activated protein kinase dependent pathway. Thus, we demonstrate, for the first time, that Csk suppression is an important early event in colorectal cancer pathogenesis. (c) 2005 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.
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