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STAT3 phosphorylation is required for the HepaCAM-mediated inhibition of castration-resistant prostate cancer cell

Bing Tan1,2,3, Xiaoming Chen4, Yanru Fan5

  • 1School of Clinical Medicine, Chongqing Medical and Pharmaceutical College, Chongqing, China.

The Prostate
|April 28, 2021
PubMed
Abstract

Insights

Hepatocyte cell adhesion molecule (HepaCAM) suppresses castration-resistant prostate cancer (CRPC) cell growth and metastasis by inhibiting the IL-22/p-STAT3 pathway. This finding offers potential therapeutic targets for advanced prostate cancer.

Area of Science:

  • Oncology
  • Molecular Biology

Background:

  • Castration-resistant prostate cancer (CRPC) is an advanced malignancy with unclear mechanisms.
  • Hepatocyte cell adhesion molecule (HepaCAM) is investigated for its role in CRPC progression.

Purpose of the Study:

  • To elucidate the function of HepaCAM in CRPC cell viability and metastasis.
  • To explore the underlying molecular mechanisms involving the IL-22/p-STAT3 axis.

Main Methods:

  • Immunohistochemistry and western blot to assess HepaCAM and p-STAT3 expression in CRPC tissues.
  • Cell proliferation, migration, and invasion assays to evaluate HepaCAM's functional impact.
  • Orthotopic xenograft mouse models to study metastasis inhibition.

Main Results:

  • HepaCAM expression was decreased, while p-STAT3 was elevated in CRPC tissues.
  • HepaCAM overexpression inhibited CRPC cell proliferation, migration, and invasion.
  • HepaCAM suppressed the IL-22/p-STAT3 axis and reduced lung metastasis in vivo.

Conclusions:

  • HepaCAM acts as a tumor suppressor in CRPC by inhibiting the IL-22/p-STAT3 pathway.
  • HepaCAM significantly reduces CRPC cell viability and metastasis to the lungs.
Keywords:
CRPCHepaCAMmetastasisp-STAT3viability

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