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JCS ePress online publication date 14 Feb 2006
doi: 10.1242/jcs.02779

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Research Article

APC inhibits ERK pathway activation and cellular proliferation induced by RAS


Ki-Sook Park, Soung Hoo Jeon, Sung-Eun Kim, Young-Yil Bahk, Sheri L. Holmen, Bart O. Williams, Kwang-Chul Chung, Young-Joon Surh, and Kang-Yell Choi*
* Author for correspondence (e-mail: kychoi{at}yonsei.ac.kr)

Inactivating mutations in the adenomatous polyposis coli gene (APC), and activating mutations in RAS, occur in a majority of colorectal carcinomas. However, the relationship between these changes and tumorigenesis is poorly understood. RAS-induced activation of the ERK pathway was reduced by overexpressing APC in DLD-1 colorectal cancer cells. ERK activity was increased by Cre-virus-induced Apc knockout in primary Apcflox/flox mouse embryonic fibroblasts, indicating that APC inhibits ERK activity. ERK activity was increased by overexpression and decreased by knock down of {beta}-catenin. The activation of Raf1, MEK and ERK kinases by {beta}-catenin was reduced by co-expression of APC. These results indicate that APC inhibits the ERK pathway by an action on {beta}-catenin. RAS-induced activation of the ERK pathway was reduced by the dominant negative form of TCF4, indicating that the ERK pathway regulation by APC/{beta}-catenin signaling is, at least, partly caused by effects on {beta}-catenin/TCF4-mediated gene expression. The GTP loading and the protein level of mutated RAS were decreased in cells with reduced ERK activity as a result of APC overexpression, indicating that APC regulates RAS-induced ERK activation at least partly by reduction of the RAS protein level. APC regulates cellular proliferation and transformation induced by activation of both RAS and {beta}-catenin signaling.
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