BCL-2 in prostate cancer: a minireview

Apoptosis. 2003 Jan;8(1):29-37. doi: 10.1023/a:1021692801278.


Prostate cancer progression and the development of androgen-independent prostate cancer have been largely related to a number of genetic abnormality that affect not only the androgen receptor but also crucial molecules involved in the regulation of survival or apoptotic pathways. One of these molecules, the pro-survival protein BCL-2, has been associated with the development of androgen-independent prostate cancer due to its high levels of expression in androgen-independent tumors in advanced stages of the pathology. The upregulation of BCL-2 after androgen ablation in prostate carcinoma cell lines and in a castrated-male rat model further established a connection between BCL-2 expression and prostate cancer progression. This review focuses on the experimental evidence that associates BCL-2 expression with prostate carcinogenesis and cancer progression, and analyzes the evidence that links the phosphatidylinositol 3-kinase (PI 3-kinase)/nuclear factor kappa B (NF-kappaB) survival pathway with the upregulation of BCL-2. The way in which hormone ablation influences this survival pathway and the potential application of novel therapeutic strategies to overcome this anti-apoptotic mechanism is examined.

Publication types

  • Research Support, U.S. Gov't, P.H.S.
  • Review

MeSH terms

  • Androgens / metabolism
  • Animals
  • Apoptosis
  • Cell Survival
  • Disease Models, Animal
  • Disease Progression
  • Humans
  • Male
  • NF-kappa B / metabolism
  • Phosphatidylinositol 3-Kinases / metabolism
  • Prostatic Neoplasms / metabolism*
  • Prostatic Neoplasms / therapy
  • Proto-Oncogene Proteins c-bcl-2 / metabolism
  • Proto-Oncogene Proteins c-bcl-2 / physiology*
  • Rats
  • Receptors, Androgen / metabolism
  • Signal Transduction
  • Tumor Necrosis Factor-alpha / metabolism
  • Up-Regulation


  • Androgens
  • NF-kappa B
  • Proto-Oncogene Proteins c-bcl-2
  • Receptors, Androgen
  • Tumor Necrosis Factor-alpha
  • Phosphatidylinositol 3-Kinases