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A New Technique for Treating Low-risk Prostate Cancer—Super Active Surveillance
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EAF2 and p53 Co-Regulate STAT3 Activation in Prostate Cancer.

Laura E Pascal1, Yao Wang2, Mingming Zhong1

  • 1Department of Urology, University of Pittsburgh School of Medicine, Pittsburgh, PA 15232, USA.

Neoplasia (New York, N.Y.)
|March 9, 2018
PubMed
Summary

Loss of tumor suppressors EAF2 and p53 promotes prostate cancer by activating the STAT3 pathway. This finding offers new insights into prostate tumorigenesis and potential therapeutic targets.

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Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Prostate cancer often involves dysregulation of tumor suppressor genes EAF2 and p53.
  • Concurrent p53 nuclear staining and EAF2 downregulation correlate with high Gleason scores in prostate cancer.

Purpose of the Study:

  • To investigate the functional interaction between EAF2 and p53 in prostate tumorigenesis.
  • To identify molecular pathways regulated by the combined loss of EAF2 and p53.

Main Methods:

  • RNA sequencing to identify genes differentially regulated by concurrent EAF2 and p53 knockdown.
  • Murine models and prostate cancer cell lines (C4-2) were used to study gene function.
  • Immunohistochemistry to assess protein expression (p-STAT3) in mouse prostate and human cancer specimens.

Main Results:

  • Concurrent knockdown of EAF2 and p53 enhanced prostate cancer cell proliferation and migration.
  • RNA-seq revealed STAT3 signaling pathway involvement, confirmed by increased p-STAT3 in Eaf2-/-p53-/- mice.
  • STAT3 knockdown reversed the proliferative effects of EAF2/p53 loss in C4-2 cells.
  • Increased p-STAT3 was observed in human prostate cancers with EAF2 downregulation and/or p53 nuclear staining.

Conclusions:

  • Simultaneous inactivation of EAF2 and p53 activates the STAT3 signaling pathway.
  • This activation contributes to the progression of prostate tumorigenesis.
  • Targeting the STAT3 pathway may offer a therapeutic strategy for prostate cancers with combined EAF2 and p53 loss.