Coiled-coil domain containing 85B suppresses the β-catenin activity in a p53-dependent manner

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Abstract
Aberrant accumulation of β-catenin is closely related to carcinogenesis. Mutations in the p53 gene are reported to induce the aberrant accumulation of β-catenin in the absence of dysfunction in the glycogen synthase kinase 3β (GSK3β)-mediated degradation pathway, but the mechanism remains incompletely understood. Here, we show that human coiled-coil domain containing 85B (CCDC85B) is induced by p53 and regulates β-catenin activity via interaction with the T-cell factor 4 in the nucleus. Moreover, CCDC85B enhances the degradation of β-catenin and suppresses tumor cell growth. In conclusion, we revealed that CCDC85B-induced degradation of β-catenin is independent of GSK3β and other p53-inducible products, Siah-1L, suggesting that CCDC85B constitutes the one of the frameworks of p53-induced multiple regulatory pathways for β-catenin activity.

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