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REPS2/POB1 is downregulated during human prostate cancer progression and inhibits growth factor signalling in

Josien K Oosterhoff1, Fred Penninkhof, Albert O Brinkmann

  • 1Department of Reproduction and Development, Erasmus MC, Erasmus University Rotterdam, PO Box 1738, 3000 DR, Rotterdam, The Netherlands.

Oncogene
|May 29, 2003
PubMed

Insights

REPS2/POB1 protein levels decrease as prostate cancer progresses, impacting growth factor signaling and cell proliferation control. This suggests REPS2/POB1 is crucial for regulating prostate cancer growth.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cellular Signaling

Background:

  • Prostate cancer progression involves a shift from androgen dependence to independence.
  • Growth factors like epidermal growth factor (EGF) become key regulators of proliferation during this transition.
  • The role of REPS2/POB1 in prostate cancer progression and growth factor signaling requires investigation.

Purpose of the Study:

  • To investigate the involvement of REPS2/POB1 in the transition of prostate cancer from androgen-dependent to androgen-independent growth.
  • To understand the function of REPS2/POB1 in growth factor signaling pathways, particularly those involving EGF.

Main Methods:

  • Expression analysis of REPS2/POB1 in androgen-dependent and independent prostate cancer cell lines and xenografts.
  • Cloning and characterization of a novel N-terminally extended form of REPS2/POB1.
  • Overexpression studies using transient transfection in prostate cancer cell lines.
  • Assessment of apoptosis induction and signaling pathway inhibition (TPA response element luciferase reporter).

Main Results:

  • REPS2/POB1 is expressed at higher levels in androgen-dependent compared to androgen-independent prostate cancer.
  • A novel, longer form of REPS2/POB1 was identified and found to be expressed in prostate cancer cells.
  • Overexpression of both REPS2/POB1 forms induced apoptosis in prostate cancer cells within 48 hours.
  • Signaling towards a TPA response element luciferase reporter was inhibited shortly after transfection.

Conclusions:

  • REPS2/POB1 influences growth factor signaling, specifically through the Ral signaling pathway.
  • Decreased REPS2/POB1 expression during prostate cancer progression may lead to dysregulated growth factor signaling.
  • This dysregulation contributes to the loss of cell proliferation control in advanced prostate cancer.

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