期刊
JOURNAL OF BIOLOGICAL CHEMISTRY
卷 282, 期 15, 页码 11221-11229出版社
AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
DOI: 10.1074/jbc.M611871200
关键词
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资金
- NCI NIH HHS [R01 CA082683, CA16672, R01 CA109035, CA82683, 1R01CA109035-01A1, CA55418, P30 CA016672] Funding Source: Medline
Increased transcriptional activity of beta-catenin resulting from Wnt/Wingless-dependent or -independent signaling has been detected in many types of human cancer, but the underlying mechanism of Wnt-independent regulation is poorly understood. We have demonstrated that AKT, which is activated downstream from epidermal growth factor receptor signaling, phosphorylates beta-catenin at Ser(552) in vitro and in vivo. AKT-mediated phosphorylation of beta-catenin causes its disassociation from cell-cell contacts and accumulation in both the cytosol and the nucleus and enhances its interaction with 14-3-3 zeta via a binding motif containing Ser(552). Phosphorylation of beta-catenin by AKT increases its transcriptional activity and promotes tumor cell invasion, indicating that AKT-dependent regulation of beta-catenin plays a critical role in tumor invasion and development.
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