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Testosterone-repressed prostate message-2 is an antiapoptotic gene involved in progression to androgen independence

H Miyake1, C Nelson, P S Rennie

  • 1The Prostate Centre, Vancouver General Hospital, British Columbia, Canada.

Cancer Research
|January 26, 2000
PubMed

Insights

Testosterone-repressed prostate message-2 (TRPM-2) is an antiapoptotic gene, not androgen-repressed. TRPM-2 overexpression confers resistance to androgen ablation, accelerating prostate cancer progression.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Endocrinology

Background:

  • The role of testosterone-repressed prostate message-2 (TRPM-2) in apoptosis has been unclear.
  • Previous studies suggested TRPM-2 might be androgen-repressed in the prostate.

Purpose of the Study:

  • To elucidate the functional role of TRPM-2 in apoptosis and its regulation by androgens.
  • To investigate TRPM-2 as a therapeutic target for prostate cancer.

Main Methods:

  • Studied TRPM-2 expression in androgen-dependent Shionogi tumors and LNCaP prostate cancer cells.
  • Utilized calcium channel blockers to inhibit castration-induced apoptosis.
  • Overexpressed TRPM-2 in LNCaP cells.
  • Administered antisense TRPM-2 oligodeoxynucleotides (ODNs) in the Shionogi tumor model.

Main Results:

  • TRPM-2 up-regulation was prevented by calcium channel blockers, indicating regulation by apoptotic stimuli, not direct androgen repression.
  • TRPM-2 overexpression in LNCaP cells led to resistance to androgen ablation in vivo.
  • Antisense TRPM-2 ODN therapy accelerated apoptosis and tumor regression post-castration.
  • TRPM-2 inhibition delayed the emergence of androgen-independent recurrent tumors.

Conclusions:

  • TRPM-2 functions as an antiapoptotic gene, promoting resistance to androgen ablation in prostate cancer.
  • TRPM-2 is a key mediator in the progression to androgen independence.
  • Targeting TRPM-2 with antisense ODNs shows therapeutic potential for overcoming androgen ablation resistance.

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