Heat shock and other apoptosis-related proteins as therapeutic targets in prostate cancer

Asian J Androl. 2014 May-Jun;16(3):359-63. doi: 10.4103/1008-682X.126400.

Abstract

Defects within apoptotic pathways have been implicated in prostate cancer (PCa) tumorigenesis, metastatic progression and treatment resistance. A hallmark of cancers is the ability to derail apoptosis by inhibiting the apoptotic signal, reducing the expression of apoptotic proteins and/or amplifying survival signals through increased production of antiapoptotic molecule. This review describes associations between heat shock proteins (HSPs) and the human androgen receptor (AR), the role of HSPs and other stress-induced proteins in PCa development and emerging strategies in targeting these protective proteins to treat PCa.

Publication types

  • Review

MeSH terms

  • Apoptosis / drug effects
  • Apoptosis / physiology
  • Apoptosis Regulatory Proteins / metabolism*
  • Clinical Trials as Topic
  • Clusterin / antagonists & inhibitors
  • Clusterin / metabolism
  • HSP27 Heat-Shock Proteins / antagonists & inhibitors
  • HSP27 Heat-Shock Proteins / metabolism
  • HSP90 Heat-Shock Proteins / antagonists & inhibitors
  • Heat-Shock Proteins / metabolism*
  • Humans
  • Male
  • Molecular Chaperones
  • Prostatic Neoplasms / drug therapy*
  • Prostatic Neoplasms / metabolism*
  • Prostatic Neoplasms / pathology
  • Prostatic Neoplasms, Castration-Resistant / drug therapy
  • Prostatic Neoplasms, Castration-Resistant / metabolism
  • Prostatic Neoplasms, Castration-Resistant / pathology
  • Proto-Oncogene Proteins c-bcl-2 / antagonists & inhibitors
  • Receptors, Androgen / metabolism
  • Signal Transduction / drug effects

Substances

  • AR protein, human
  • Apoptosis Regulatory Proteins
  • CLU protein, human
  • Clusterin
  • HSP27 Heat-Shock Proteins
  • HSP90 Heat-Shock Proteins
  • HSPB1 protein, human
  • Heat-Shock Proteins
  • Molecular Chaperones
  • Proto-Oncogene Proteins c-bcl-2
  • Receptors, Androgen