Akt in prostate cancer: Possible role in androgen-independence

Paramita M. Ghosh, Shazli Malik, Roble Bedolla, Jeffrey I. Kreisberg

Research output: Contribution to journalReview articlepeer-review

81 Scopus citations


Akt, a downstream effector of phosphatidylinositol 3-kinase (P13K), has often been implicated in prostate cancer. Studies in prostate tumor cell lines revealed that Akt activation is probably important for the progression of prostate cancer to an androgen-independent state. Investigations of human prostate cancer tissues show that although there is neither Akt gene amplification nor enhanced protein expression in prostate cancer compared to normal tissue, poorly differentiated tumors exhibit increased expression of a phosphorylated (activated) form of Akt compared to normal tissue, prostatic intraepithelial neoplasia (PIN) or well-differentiated prostate cancer. Akt phosphorylation is accompanied by the inactivation of ERK, a member of the mitogen activated protein kinase (MAPK) family. In this article, we postulate that Akt promotes androgen-independent survival of prostate tumor cells by modulating the expression and activation of the androgen receptor (AR).

Original languageEnglish (US)
Pages (from-to)487-496
Number of pages10
JournalCurrent Drug Metabolism
Issue number6
StatePublished - Dec 2003
Externally publishedYes


  • Akt
  • Androgen receptor
  • MAPK
  • PI3K
  • Prostate cancer
  • PTEN

ASJC Scopus subject areas

  • Pharmacology
  • Clinical Biochemistry


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