Prostate cancer cells use genetic and epigenetic mechanisms for progression to androgen independence Academic Article uri icon


MeSH Major

  • Androgens
  • Epigenesis, Genetic
  • Prostatic Neoplasms


  • 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

publication date

  • July 2006



  • Academic Article



  • eng

Digital Object Identifier (DOI)

  • 10.1002/gcc.20333

PubMed ID

  • 16615098

Additional Document Info

start page

  • 702

end page

  • 16


  • 45


  • 7