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Akt in prostate cancer: possible role in androgen-independence

Paramita M Ghosh1, Shazli Malik, Roble Bedolla

  • 1Department of Surgery, University of Texas Health Science Center at San Antonio and South Texas Veterans Health Care System, Audie L. Murphy Veterans Administration Hospital, San Antonio, TX 78229-3900, USA.

Current Drug Metabolism
|December 20, 2003
PubMed

Insights

Activated Akt (a protein kinase) promotes prostate cancer progression to an androgen-independent state. This occurs through modulation of the androgen receptor (AR), impacting tumor cell survival.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Akt, a key downstream effector of PI3K, is frequently implicated in prostate cancer.
  • Akt activation is crucial for prostate cancer progression toward androgen independence.

Purpose of the Study:

  • To investigate the role of Akt activation in prostate cancer progression.
  • To explore the mechanism by which Akt promotes androgen-independent survival of prostate tumor cells.

Main Methods:

  • Analysis of Akt expression and phosphorylation in human prostate cancer tissues.
  • Comparison of Akt activation in normal tissue, PIN, and various grades of prostate cancer.
  • Investigation of the relationship between Akt phosphorylation and ERK inactivation.

Main Results:

  • No Akt gene amplification or increased total protein expression in prostate cancer versus normal tissue.
  • Significantly increased phosphorylated (activated) Akt in poorly differentiated tumors compared to normal tissue, PIN, and well-differentiated cancers.
  • Akt phosphorylation correlated with ERK inactivation.

Conclusions:

  • Akt activation, not increased expression, is associated with advanced prostate cancer.
  • Akt may promote androgen-independent prostate cancer cell survival by modulating androgen receptor (AR) expression and activation.

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