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

Horacio Murillo, Lucy J. Schmidt, Melissa Karter, Kari A. Hafner, Yasushi Kondo, Karla V. Ballman, George Vasmatzis, Robert B. Jenkins, Donald J. Tindall

Research output: Contribution to journalArticlepeer-review

14 Scopus citations

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.

Original languageEnglish (US)
Pages (from-to)702-716
Number of pages15
JournalGenes Chromosomes and Cancer
Volume45
Issue number7
DOIs
StatePublished - Jul 2006

ASJC Scopus subject areas

  • Genetics
  • Cancer Research

Fingerprint Dive into the research topics of 'Prostate cancer cells use genetic and epigenetic mechanisms for progression to androgen independence'. Together they form a unique fingerprint.

Cite this