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Loss of the SSeCKS/Gravin/AKAP12 gene results in prostatic hyperplasia

Shin Akakura1, Changhui Huang, Peter J Nelson

  • 1Department of Cancer Genetics, Therapeutics Roswell Park Cancer Institute, Buffalo, New York 14263, USA.

Cancer Research
|July 3, 2008
PubMed

Insights

Loss of SSeCKS (a metastasis suppressor) in mice causes prostate hyperplasia and increased apoptosis. This suggests SSeCKS is crucial for maintaining prostate health and preventing cancer development.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • SSeCKS/Gravin/AKAP12 (SSeCKS) is a kinase scaffolding protein with metastasis-suppressor activity.
  • SSeCKS down-regulates Src-mediated oncogenic signaling and vascular endothelial growth factor expression.
  • Reduced SSeCKS expression is observed in various cancers, including prostate cancer.

Purpose of the Study:

  • To investigate the role of SSeCKS in prostate homeostasis and oncogenic transformation.
  • To determine the effects of SSeCKS loss on prostate tissue structure and signaling pathways.

Main Methods:

  • Analysis of SSeCKS expression in normal and cancerous prostate tissues.
  • Phenotypic characterization of SSeCKS-null mouse prostates, including hyperplasia and apoptosis.
  • Assessment of molecular markers such as E-cadherin, cytokeratins, and AKT phosphorylation.

Main Results:

  • SSeCKS loss in mice leads to prostatic hyperplasia in specific lobes and increased apoptosis.
  • Dysplastic foci in SSeCKS-null prostates show loss of E-cadherin and basal epithelial cells.
  • SSeCKS-null prostate tissues exhibit elevated AKT(poS473) levels, indicating attenuated phosphatidylinositol-3-OH kinase signaling.

Conclusions:

  • SSeCKS plays a critical role in maintaining prostate epithelial cell differentiation and survival.
  • The loss of SSeCKS function promotes prostate hyperplasia and increases susceptibility to oncogenic transformation.
  • SSeCKS acts as a suppressor of phosphatidylinositol-3-OH kinase signaling in the prostate.

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