Prostate cancer cells use genetic and epigenetic mechanisms for progression to androgen independence

Genes Chromosomes Cancer. 2006 Jul;45(7):702-16. doi: 10.1002/gcc.20333.

Abstract

Studies on the genetic basis of prostate cancer (PCa) have lead to mixed results with the only consensus being that PCa is a complex disease. Our goal was to gain insight into potential events involved in the acquisition of the androgen-refractory phenotype in PCa cells regardless of DNA-change dependence. To this end, we examined two LNCaP PCa cell line models of progression-one developed in vivo and one developed in vitro-using molecular cytogenetic and microarray gene expression analyses and extended this investigation of specific events into PCa tumors. The chromosomal changes observed in both in vivo and in vitro androgen-independent cell lines are similar to those seen in PCa during tumor progression. Correspondingly, gene expression analysis showed significant heterogeneity in the genes expressed among androgen-independent cells, but with some common gene expression changes that correlated with the acquired androgen-independent phenotype. Thus, growth conditions under which the cells progress appeared to impact the mechanisms used for progression, albeit within tumor-type-specific pathways. Our findings suggest that a dynamic and adaptable combination of epigenetic and DNA-change-dependent events can be used by PCa cells for the acquisition of the androgen-independent phenotype. This article contains Supplementary Material available at http://www.interscience.wiley.com/jpages/1045-2257/suppmat.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Androgens / metabolism*
  • Animals
  • Cell Line, Tumor
  • Chromosome Banding
  • DNA-Binding Proteins / genetics
  • Epigenesis, Genetic*
  • Gene Expression Regulation, Neoplastic
  • Humans
  • In Situ Hybridization, Fluorescence
  • Loss of Heterozygosity
  • Male
  • Mice
  • Oligonucleotide Array Sequence Analysis
  • Phenotype
  • Prostatic Neoplasms / genetics*
  • Prostatic Neoplasms / metabolism
  • Spectral Karyotyping

Substances

  • Androgens
  • DNA-Binding Proteins
  • PLAG1 protein, human