Chronic azacitidine treatment results in differentiating effects, sensitizes against bicalutamide in androgen-independent prostate cancer cells

Prostate. 2008 May 15;68(7):793-801. doi: 10.1002/pros.20748.

Abstract

Background: About 20-30% of hormone-independent PCa are characterized by the extensive loss of AR expression that appears to occur at the transcriptional level. Treatment of AR-negative PCa cells with demethylating agents (Aza-CR) leads to expression of AR mRNA and protein. Here, we investigate the effect of Aza-CR administered both acutely and chronically on AR expression, PSA expression, cell survival, and proliferation in androgen-independent/AR-negative PCa cells. We also studied whether epigenetically reactivated AR is a target for bicalutamide therapy.

Methods: The in vitro effect of Aza-CR as single agent and its ability to induce AR expression and to augment the efficacy to bicalutamide were assessed using two androgen-independent and AR-negative cell lines (PC3 and DU145).

Results: Our results show that acute treatment (4 days) with Aza-CR results in a relatively low decrease in cell proliferation with G2 cell cycle arrest and no significant evidence of apoptosis or AR expression. Interestingly, when Aza-CR was chronically administered (20 days), this treatment resulted in marked decrease in tumor cell proliferation with significant increase in AR and PSA protein levels. Furthermore, following Aza-CR chronic treatment the formerly androgen-independent PC3 and DU145 cells increase their susceptibility to the apoptotic effects of bicalutamide.

Conclusions: Aza-CR acute treatment has modest effects on androgen-independent and AR-negative PCa cell survival and proliferation, but chronic administration results in profound decrease in proliferation and in sensitization to antiandrogen agents. All these effects seem, in some measure, dependent on a partial restoration of androgen regulation.

MeSH terms

  • Androgen Antagonists / pharmacology*
  • Androgens / metabolism
  • Anilides / pharmacology*
  • Antineoplastic Agents / pharmacology*
  • Apoptosis / drug effects
  • Azacitidine / pharmacology*
  • Cell Cycle / drug effects
  • Cell Line, Tumor
  • Cell Survival / drug effects
  • Gene Silencing
  • Humans
  • Male
  • Nitriles / pharmacology*
  • Prostate-Specific Antigen / metabolism
  • Prostatic Neoplasms / drug therapy*
  • Prostatic Neoplasms / metabolism
  • Prostatic Neoplasms / pathology
  • RNA, Small Interfering / metabolism
  • Receptors, Androgen / genetics
  • Receptors, Androgen / metabolism
  • Repressor Proteins / genetics
  • Repressor Proteins / metabolism
  • Tosyl Compounds / pharmacology*

Substances

  • Androgen Antagonists
  • Androgens
  • Anilides
  • Antineoplastic Agents
  • DMAP1 protein, human
  • Nitriles
  • RNA, Small Interfering
  • Receptors, Androgen
  • Repressor Proteins
  • Tosyl Compounds
  • bicalutamide
  • Prostate-Specific Antigen
  • Azacitidine