FoxM1 promotes β-catenin nuclear localization and controls Wnt target-gene expression and glioma tumorigenesis.

Abstract:

:Wnt/β-catenin signaling is essential for stem cell regulation and tumorigenesis, but its molecular mechanisms are not fully understood. Here, we report that FoxM1 is a downstream component of Wnt signaling and is critical for β-catenin transcriptional function in tumor cells. Wnt3a increases the level and nuclear translocation of FoxM1, which binds directly to β-catenin and enhances β-catenin nuclear localization and transcriptional activity. Genetic deletion of FoxM1 in immortalized neural stem cells abolishes β-catenin nuclear localization. FoxM1 mutations that disrupt the FoxM1-β-catenin interaction or FoxM1 nuclear import prevent β-catenin nuclear accumulation in tumor cells. FoxM1-β-catenin interaction controls Wnt target gene expression, is required for glioma formation, and represents a mechanism for canonical Wnt signaling during tumorigenesis.

journal_name

Cancer Cell

journal_title

Cancer cell

authors

Zhang N,Wei P,Gong A,Chiu WT,Lee HT,Colman H,Huang H,Xue J,Liu M,Wang Y,Sawaya R,Xie K,Yung WK,Medema RH,He X,Huang S

doi

10.1016/j.ccr.2011.08.016

subject

Has Abstract

pub_date

2011-10-18 00:00:00

pages

427-42

issue

4

eissn

1535-6108

issn

1878-3686

pii

S1535-6108(11)00312-6

journal_volume

20

pub_type

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