TRAF4 participates in Wnt/β-catenin signaling in breast cancer by upregulating β-catenin and mediating its translocation to the nucleus

Mol Cell Biochem. 2014 Oct;395(1-2):211-9. doi: 10.1007/s11010-014-2127-y. Epub 2014 Jul 3.

Abstract

Tumor necrosis factor receptor-associated factor 4 (TRAF4) is upregulated in various subtypes of breast cancers and cell lines; however, the precise functions of TRAF4 are poorly understood. Our objective was to investigate its relationship with β-catenin. TRAF4 participates in several signaling pathways, such as NF-κB and JNK signaling pathways. In this study, we identified β-catenin as a TRAF4-binding protein, have shown that TRAF4 enhanced expression of β-catenin, and found that TRAF4 mediated the translocation of β-catenin from the cytoplasm to the nucleus, thereby facilitating activation of the Wnt signaling pathway in breast cancer.

MeSH terms

  • Active Transport, Cell Nucleus*
  • Breast Neoplasms / genetics
  • Breast Neoplasms / metabolism*
  • Cell Line, Tumor
  • Cell Nucleus / metabolism
  • Female
  • Gene Expression Regulation, Neoplastic
  • Humans
  • MCF-7 Cells
  • TNF Receptor-Associated Factor 4 / genetics
  • TNF Receptor-Associated Factor 4 / metabolism*
  • Up-Regulation
  • Wnt Signaling Pathway*
  • beta Catenin / metabolism*

Substances

  • CTNNB1 protein, human
  • TNF Receptor-Associated Factor 4
  • TRAF4 protein, human
  • beta Catenin