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Updated: Aug 7, 2026

An Orthotopic Murine Model of Human Prostate Cancer Metastasis
06:48

An Orthotopic Murine Model of Human Prostate Cancer Metastasis

Published on: September 18, 2013

The Src-suppressed C kinase substrate, SSeCKS, is a potential metastasis inhibitor in prostate cancer

W Xia1, P Unger, L Miller

  • 1Departments of Microbiology, Mount Sinai School of Medicine, New York, New York 10029-6574, USA.

Cancer Research
|July 17, 2001
PubMed

Insights

Loss of SSeCKS/Gravin, a tumor suppressor, is linked to prostate cancer metastasis. Reintroducing SSeCKS/Gravin reduced tumor growth and significantly decreased lung metastases in preclinical models.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Genetics

Background:

  • Prostate cancer progression and metastasis mechanisms are not fully understood.
  • SSeCKS/Gravin, a protein kinase scaffolding protein, exhibits tumor suppressor activity.
  • The gene for Gravin/AKAP12 is located at 6q24-25.2, a region frequently deleted in advanced prostate cancer.

Purpose of the Study:

  • Investigate the role of SSeCKS/Gravin in prostate cancer development and metastasis.
  • Determine SSeCKS/Gravin expression patterns in normal and cancerous prostate tissues and cell lines.
  • Evaluate the therapeutic potential of SSeCKS/Gravin reexpression in preclinical models.

Main Methods:

  • Western blot and RT-PCR to assess SSeCKS/Gravin protein and RNA levels.
  • Cell culture experiments involving reexpression of SSeCKS in prostate cancer cell lines.
  • In vivo studies using nude mice to evaluate tumor growth and metastasis.
  • Immunohistochemical analysis of SSeCKS/Gravin expression in human prostate lesions.

Main Results:

  • SSeCKS/Gravin protein and RNA were detected in normal prostate epithelial cells but severely reduced in prostate cancer cell lines.
  • Reexpression of SSeCKS in cancer cells induced morphological changes and reduced anchorage-independent growth.
  • SSeCKS reexpression in vivo decreased primary tumor growth and significantly reduced lung metastasis formation.
  • Loss of SSeCKS/Gravin expression correlated with undifferentiated prostate carcinomas and advanced disease.

Conclusions:

  • Loss of SSeCKS/Gravin contributes to prostate cancer progression and metastasis.
  • SSeCKS/Gravin functions as a tumor suppressor in prostate cancer.
  • Restoring SSeCKS/Gravin levels may represent a potential therapeutic strategy for metastatic prostate cancer.

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