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RhoC GTPase Activation Assay
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SOX11-induced decrease in vimentin and an increase in prostate cancer cell migration attributed to cofilin activity.

Yoshifumi S Hirokawa1, Kazuki Kanayama2, Michiko Kagaya1

  • 1Department of Oncologic Pathology, Mie University Graduate School of Medicine, Tsu, Mie 514-8507, Japan.

Experimental and Molecular Pathology
|September 24, 2020
PubMed
Summary

SOX11 promotes prostate cancer progression by inducing an epithelial phenotype and enhancing cell migration. Increased SOX11 gene amplification in metastatic tumors suggests its role in advanced prostate cancer.

Keywords:
CofilinKeratin 18MMP2Prostate cancerSOX11

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Area of Science:

  • Molecular Biology
  • Cancer Research
  • Genetics

Background:

  • SOX11 is a transcription factor regulating cellular events in development and tumorigenesis.
  • Its role in prostate cancer progression remains to be fully elucidated.

Purpose of the Study:

  • To investigate the function of SOX11 in prostate cancer cells.
  • To determine the impact of SOX11 overexpression on cellular phenotype and migratory properties.

Main Methods:

  • Prostate cancer PC-3 cells were engineered for high SOX11 expression (S6 and S9 clones).
  • Changes in epithelial and mesenchymal markers were assessed.
  • Cell migration assays were performed.
  • Analysis of The Cancer Genome Atlas (TCGA) dataset for SOX11 gene amplification in prostate tumors.

Main Results:

  • SOX11 overexpression induced an epithelial phenotype, characterized by loss of vimentin and gain of epithelial markers.
  • SOX11-expressing cells exhibited increased migratory properties.
  • Enhanced migration was linked to cofilin activity and keratin 18 expression.
  • TCGA data showed higher SOX11 gene amplification in metastatic prostate tumors compared to primary tumors.

Conclusions:

  • SOX11 plays a tumor-promotive role in prostate cancer.
  • SOX11 induces epithelial protein expression and enhances cell migration.
  • SOX11 may be a significant factor in prostate cancer metastasis.