FoxM1 Promotes β-Catenin Nuclear Localization and Controls Wnt Target-Gene Expression and Glioma Tumorigenesis

Nu Zhang, Ping Wei, Aihua Gong, Wen Tai Chiu, Hsueh Te Lee, Howard Colman, He Huang, Jianfei Xue, Mingguang Liu, Yong Wang, Raymond Sawaya, Keping Xie, W. K.Alfred Yung, René H. Medema, Xi He, Suyun Huang

研究成果: Article同行評審

394 引文 斯高帕斯(Scopus)

摘要

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.

原文English
頁(從 - 到)427-442
頁數16
期刊Cancer Cell
20
發行號4
DOIs
出版狀態Published - 2011 10月 18

All Science Journal Classification (ASJC) codes

  • 腫瘤科
  • 細胞生物學
  • 癌症研究

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