SGEF is overexpressed in prostate cancer and contributes to prostate cancer progression

Oncol Rep. 2012 Oct;28(4):1468-74. doi: 10.3892/or.2012.1917. Epub 2012 Jul 19.

Abstract

The purpose of this study was to investigate the potential roles of the SH3-containing guanine nucleotide exchange factor (SGEF) in human prostate cancer. Experimental data showed that SGEF was overexpressed in human prostate cancer cells and specimens. The reduction of SGEF expression through an SGEF-targeting siRNA in androgen-independent C4-2 and C4-2B cells suppressed both anchorage-dependent and anchorage-independent growth. In addition, the androgen receptor (AR) antagonist bicalutamide further strengthened this inhibitory effect due to the suppression of the elevated AR transactivation after knockdown of SGEF. Collectively, our results provide the first demonstration that SGEF is a novel promoter of human prostate cancer progression and development.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Androgen Receptor Antagonists / pharmacology
  • Anilides / pharmacology
  • Gene Expression Regulation, Neoplastic
  • Gene Knockdown Techniques
  • Guanine Nucleotide Exchange Factors / genetics*
  • Guanine Nucleotide Exchange Factors / metabolism
  • Humans
  • Male
  • Nitriles / pharmacology
  • Prostatic Neoplasms / drug therapy
  • Prostatic Neoplasms / genetics*
  • Prostatic Neoplasms / metabolism
  • Prostatic Neoplasms / pathology*
  • Proto-Oncogene Proteins c-akt / metabolism
  • RNA, Small Interfering
  • Receptors, Androgen / genetics
  • Receptors, Androgen / metabolism
  • Signal Transduction
  • Tosyl Compounds / pharmacology
  • Transcriptional Activation
  • Tumor Cells, Cultured

Substances

  • ARHGEF26 protein, human
  • Androgen Receptor Antagonists
  • Anilides
  • Guanine Nucleotide Exchange Factors
  • Nitriles
  • RNA, Small Interfering
  • Receptors, Androgen
  • Tosyl Compounds
  • bicalutamide
  • Proto-Oncogene Proteins c-akt