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FGF-2 disrupts mitotic stability in prostate cancer through the intracellular trafficking protein CEP57

Rolando Cuevas1, Nina Korzeniewski, Yanis Tolstov

  • 1Cancer Virology Program, University of Pittsburgh Cancer Institute, Pittsburgh, PA, USA.

Cancer Research
|December 18, 2012
PubMed

Insights

Fibroblast growth factor 2 (FGF-2) overexpression causes prostate cancer cells to mismanage centrosome duplication via CEP57, leading to aneuploidy. Targeting the FGF-2/FGFR1/CEP57 pathway may offer new prostate cancer therapies.

Area of Science:

  • Cell Biology
  • Cancer Biology
  • Molecular Oncology

Background:

  • Malignant tumors, including prostate cancer, often exhibit aneuploidy, a condition linked to errors in cell division.
  • The precise mechanisms connecting fibroblast growth factor 2 (FGF-2) overexpression to chromosome missegregation have remained unclear.

Purpose of the Study:

  • To investigate the link between FGF-2 overexpression and aneuploidy in prostate cancer.
  • To elucidate the role of CEP57 in FGF-2-mediated centrosome duplication and mitotic instability.

Main Methods:

  • Utilized RNA interference screening to identify factors regulating centriole duplication.
  • Examined the effects of FGF-2 and CEP57 overexpression on centrosome duplication and cell division in prostate cancer cells.
  • Assessed tubulin acetylation levels and CEP57 expression in prostate cancer tissues.

Main Results:

  • FGF-2 rapidly decouples centrosome duplication from the cell cycle through CEP57.
  • CEP57 overexpression leads to centriole overduplication and mitotic defects.
  • CEP57 modulates tubulin acetylation, influencing daughter centriole stability.
  • CEP57 is overexpressed in a subset of prostate cancers with concurrent FGF-2 upregulation.

Conclusions:

  • Demonstrates an unexpected link between FGF-2 signaling and mitotic instability in prostate cancer.
  • Identifies CEP57 as a key mediator of FGF-2-induced centrosome abnormalities.
  • Suggests the FGF-2/FGFR1/CEP57 axis as a potential therapeutic target for prostate cancer.

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