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A Bioluminescent and Fluorescent Orthotopic Syngeneic Murine Model of Androgen-dependent and Castration-resistant Prostate Cancer
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Glycogen synthesis correlates with androgen-dependent growth arrest in prostate cancer

Joachim B Schnier1, Kayoko Nishi, Paul H Gumerlock

  • 1Department of Biochemistry and Molecular Medicine, University of California, One Shields Avenue, Davis, CA 95616, USA. jbschnier@ucdavis.edu

BMC Urology
|March 26, 2005
PubMed
Abstract

Insights

Androgen signaling increases prostate cancer cell glycogen. Inhibiting glycogen breakdown with CP-91149 enhances this effect, reducing cell survival and recurrence risk.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Androgen withdrawal in prostate cancer reduces glucose metabolism.
  • Glycogen metabolism's role in androgen response is unstudied.

Purpose of the Study:

  • Investigate androgen's effects on glycogen metabolism in prostate cancer cells.
  • Determine if targeting glycogen metabolism impacts androgen response.

Main Methods:

  • Utilized androgen receptor (AR)-reconstituted PC3 and LNCaP cell lines.
  • Measured glycogen phosphorylase (GP) and glycogen synthase (GS) activity.
  • Assessed glycogen content and cell number following androgen treatment and GP inhibition.

Main Results:

  • Androgen increased glycogen content 2-5 fold in PC3 cells, accompanied by G1 arrest and cell reduction.
  • Androgen elevated Glucose-6-P, GS, and GP activity.
  • GP inhibition (CP-91149) enhanced glycogen accumulation and reduced cell number in both cell lines.

Conclusions:

  • Increased glycogenesis is an androgen receptor-mediated response.
  • Blocking glycogenolysis via GP inhibition potentiates androgen's anti-proliferative effect.
  • Combined GP inhibition and hormone therapy may improve prostate cancer treatment efficacy.

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