An in vitro model for preclinical testing of endocrine therapy combinations for prostate cancer

Prostate. 2010 Oct 1;70(14):1524-32. doi: 10.1002/pros.21187.

Abstract

Background: Even though patients with prostate cancer commonly respond to endocrine treatment, in most cases the disease progresses to castration resistant prostate cancer (CRPC). Our objective was to generate a novel cell line model representing the endocrine treatment naive prostate cancer for testing treatments that target the androgen receptor (AR) and androgen metabolism.

Methods: After culturing DuCaP cells 20 passages with additional 1 nM R1881, DuCaP-N(aive) cell line was developed and validated for testing endocrine therapy combinations. Cell viability, apoptosis and cell cycle distribution were assessed in DuCaP and DuCaP-N when interfering with the hormonal content.

Results: Addition of 1 nM R1881 to DuCaP reduces cell viability and induces cell cycle inhibition and apoptosis. Eventually, an androgen accustomed DuCaP-N cell line developed. An antiandrogen (bicalutamide), a histone deacetylase (HDAC) inhibitor (trichostatin A) and a 5alpha-reductase (SRD5A) inhibitor (finasteride) reduce cell viability, and their combinations give a synergistic response in inducing apoptosis.

Conclusions: The TMPRSS2-ERG expressing DuCaP-N cell line represents human prostate cancer prior to endocrine treatment, and its parental DuCaP cell line is a model for CRPC. These cell lines can be used for preclinical evaluation of compounds that target the androgenic pathway.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Androgen Antagonists / therapeutic use*
  • Androgens / pharmacology
  • Androgens / therapeutic use
  • Animals
  • Apoptosis
  • Cell Cycle
  • Cell Line, Tumor
  • Cell Survival
  • Cholesterol Side-Chain Cleavage Enzyme / genetics
  • DNA Primers
  • Disease Progression
  • Finasteride / therapeutic use*
  • Humans
  • In Situ Hybridization, Fluorescence
  • Male
  • Mice
  • Mice, SCID
  • Polymerase Chain Reaction / methods
  • Prostatic Neoplasms / drug therapy*
  • Prostatic Neoplasms / genetics
  • Prostatic Neoplasms / metabolism
  • Prostatic Neoplasms / pathology
  • RNA, Messenger / genetics
  • Serine Endopeptidases / genetics
  • Steroids / therapeutic use

Substances

  • Androgen Antagonists
  • Androgens
  • DNA Primers
  • RNA, Messenger
  • Steroids
  • Finasteride
  • Cholesterol Side-Chain Cleavage Enzyme
  • Serine Endopeptidases
  • TMPRSS2 protein, human