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SOX4 interacts with plakoglobin in a Wnt3a-dependent manner in prostate cancer cells

Yu-Heng Lai1, Jessica Cheng, Dongmei Cheng

  • 1Department of Pathology & Laboratory Medicine, Emory University School of Medicine, Atlanta, GA 30322, USA.

BMC Cell Biology
|November 22, 2011
PubMed
Abstract

Insights

Researchers identified a new inhibitory interaction between SOX4 and junction plakoglobin (JUP). This SOX4-JUP complex impacts Wnt pathway gene expression and SOX4

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Proteomics

Background:

  • SOX4 is a transcription factor crucial for tissue development, differentiation, and proliferation.
  • SOX4 overexpression is observed in numerous human cancers, but its exact role in cancer progression remains unclear.
  • Identifying SOX4 binding partners is key to understanding its function in cancer.

Purpose of the Study:

  • To identify novel SOX4 binding partners using large-scale proteomics.
  • To elucidate the functional consequences of SOX4 interactions in cancer cells.

Main Methods:

  • Adapted a one-step affinity purification method involving intracellular biotinylation of SOX4.
  • Performed large-scale proteomics analysis to identify SOX4-interacting proteins.
  • Investigated SOX4-plakoglobin interactions in prostate and breast cancer cells under various conditions (WNT3A stimulation, LMB treatment).

Main Results:

  • Discovered that junction plakoglobin (JUP) interacts with SOX4 in both the cytosol and nucleus.
  • SOX4-JUP interaction is enhanced by WNT3A stimulation and leptomycin B (LMB), suggesting plakoglobin promotes SOX4 nuclear export.
  • The SOX4-JUP complex modulates Wnt pathway target genes (e.g., AXIN2) and SOX4 targets (e.g., DICER1, DHX9), reducing SOX4 DNA binding and transcriptional activity.

Conclusions:

  • The newly identified SOX4-plakoglobin interaction is inhibitory.
  • This interaction provides novel insights into SOX4's role in cell proliferation, development, and cancer progression.
  • SOX4-JUP interaction influences key pathways involved in cancer.

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