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BCL2 antisense transcripts decrease intracellular Bcl2 expression and sensitize LNCaP prostate cancer cells to

X B Shi1, P H Gumerlock, J T Muenzer

  • 1Dept of Urology, University of California, Davis, School of Medicine, 4860 Y Street, Suite 3500, Sacramento, CA 95817, USA.

Cancer Biotherapy & Radiopharmaceuticals
|January 5, 2002
PubMed
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Down-regulating Bcl2 protein expression in prostate cancer (CaP) cells using BCL2 antisense transcripts inhibits CaP cell growth and increases sensitivity to apoptosis. This approach may offer a new therapy for advanced CaP.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Genetics

Background:

  • Prostate cancer (CaP) is a leading cause of cancer death in aging men.
  • Currently, no effective treatments exist for hormone-independent CaP.
  • Bcl2 protein is implicated in protecting CaP cells from programmed cell death (apoptosis).

Purpose of the Study:

  • To investigate the effects of down-regulating Bcl2 expression on prostate cancer cells.
  • To assess the therapeutic potential of targeting Bcl2 in advanced CaP.

Main Methods:

  • Established genetically engineered LNCaP sublines by transfecting with BCL2 antisense (BCL2-AS) transcript-expressing plasmids.
  • Utilized Western blotting to quantify intracellular Bcl2 protein levels.
  • Evaluated cell growth inhibition under androgen withdrawal and sensitivity to Adriamycin-induced apoptosis.

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Main Results:

  • BCL2-AS transfection reduced intracellular Bcl2 protein by 50-60%.
  • Antisense transcript expression led to 50% growth inhibition of LNCaP cells during androgen withdrawal.
  • BCL2-AS significantly sensitized LNCaP cells to Adriamycin-induced apoptosis.

Conclusions:

  • Down-regulation of Bcl2 protein via BCL2-AS transcripts effectively inhibits prostate cancer cell growth.
  • Targeting Bcl2 expression enhances apoptosis sensitivity in CaP cells.
  • BCL2-AS transcripts represent a potential therapeutic strategy for advanced prostate cancer.