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Hepsin inhibits CDK11p58 IRES activity by suppressing unr expression and eIF-2α phosphorylation in prostate cancer

Chunyi Zhang1, Mingming Zhang1, Qingyu Wu2

  • 1Gene Research Center, Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Fudan University, Shanghai 200032, China.

Cellular Signalling
|January 11, 2015
PubMed

Insights

Hepsin, a protein overexpressed in prostate cancer (PCa), inhibits cell cycle progression by suppressing CDK11p58 expression. This occurs through regulating translation machinery, impacting cell survival in PCa.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Biochemistry

Background:

  • Hepsin is a type II transmembrane serine protease.
  • Hepsin is frequently overexpressed in prostate cancer (PCa).
  • The precise role of hepsin in PCa pathogenesis is not fully understood.

Purpose of the Study:

  • To elucidate the function of hepsin in prostate cancer.
  • To investigate the molecular mechanisms by which hepsin influences PCa cell behavior.

Main Methods:

  • Investigated hepsin's effect on CDK11p58 expression via internal ribosome entry site (IRES) activity.
  • Analyzed the modulation of unr expression and eIF-2α phosphorylation by hepsin.
  • Examined hepsin's interaction with the unr IRES element and its impact on GCN2 signaling.

Main Results:

  • Hepsin was found to inhibit CDK11p58 IRES activity and expression in PCa cells.
  • Hepsin suppressed CDK11p58 IRES activity by modulating unr expression and eIF-2α phosphorylation.
  • Hepsin inhibited unr expression by binding to its IRES element and repressed eIF-2α phosphorylation via GCN2 pathway regulation.

Conclusions:

  • Hepsin plays a novel role in regulating CDK11p58 IRES activity in prostate cancer.
  • Hepsin may influence PCa cell cycle progression and survival by targeting translational machinery.
Keywords:
CDK11p58HepsinIRESeIF-2αunr

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