Inhibition of PAX2 expression results in alternate cell death pathways in prostate cancer cells differing in p53 status

Cancer Lett. 2007 Apr 18;248(2):251-61. doi: 10.1016/j.canlet.2006.08.007. Epub 2006 Sep 25.

Abstract

Inhibition of apoptosis is a critical pathophysiological factor that contributes to the development of prostate cancer. Recently, PAX2, a transcriptional regulator implicated in oncogenesis, has been demonstrated to be expressed by prostate cancer. However, its downstream molecular pathways for suppression of apoptosis, other than the tumor suppressor gene p53, have yet to be elucidated. Here, we examine the effects of inhibiting PAX2 expression by prostate cancer cells that differ in p53 gene status. These data collectively demonstrate that PAX2 inhibition results in cell death independent of p53, and that additional tumor suppressors or cell death pathways may be inhibited by PAX2 in prostate cancer cells.

Publication types

  • Research Support, N.I.H., Extramural

MeSH terms

  • Blotting, Western
  • Caspases / metabolism
  • Cell Death / physiology*
  • Cell Line, Tumor
  • Humans
  • Male
  • Microscopy, Confocal
  • PAX2 Transcription Factor / antagonists & inhibitors
  • PAX2 Transcription Factor / biosynthesis*
  • Prostatic Neoplasms / genetics
  • Prostatic Neoplasms / metabolism*
  • RNA, Small Interfering
  • Reverse Transcriptase Polymerase Chain Reaction
  • Tumor Suppressor Protein p53 / metabolism*

Substances

  • PAX2 Transcription Factor
  • PAX2 protein, human
  • RNA, Small Interfering
  • Tumor Suppressor Protein p53
  • Caspases