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BCL-2 in prostate cancer: A minireview

Academic Article
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Overview

authors

  • Catz, Sergio
  • Johnson, J. L.

publication date

  • January 2003

journal

  • Apoptosis  Journal

abstract

  • 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.

subject areas

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

keywords

  • NF-kappa B
  • PI 3-kinase
  • TNF alpha
  • androgens
  • apoptosis
  • survival
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Identity

International Standard Serial Number (ISSN)

  • 1360-8185

Digital Object Identifier (DOI)

  • 10.1023/a:1021692801278

PubMed ID

  • 12510149
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Additional Document Info

start page

  • 29

end page

  • 37

volume

  • 8

issue

  • 1

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