Mechanisms of action of novel agents for prostate cancer chemoprevention

Endocr Relat Cancer. 2006 Sep;13(3):751-78. doi: 10.1677/erc.1.01126.


Despite advances in the understanding of prostate cancer (PCa) growth and development, it is still the leading incidence of cases and the second leading cause of mortality due to cancer in men. The problem of early diagnosis compounded with the emergence of androgen independence during commonly used anti-androgen therapy of PCa, have been discouraging for optimal therapeutic response. Recently, many chemopreventive agents, including silibinin, inositol hexaphosphate, decursin, apigenin, acacetin, grape seed extract, curcumin, and epigallocatechin-3 gallate have been identified in laboratory studies, which could be useful in the management of PCa. In vivo pre-clinical studies have indicated chemopreventive effect of many such agents in PCa xenograft and transgenic mouse models. The molecular targets of these agents include cell signaling, cell-cycle regulators, and survival/apoptotic molecules, which are implicated in uncontrolled PCa growth and progression. Furthermore, angiogenic and metastatic targets, including vascular endothelial growth factor, hypoxia-inducing factor-1alpha, matrix metalloproteinase, and urokinase-type plasminogen activator are also modulated by many chemopreventive agents to suppress the growth and invasive potential of PCa. This review focuses on novel PCa chemopreventive observations in laboratory studies, which could provide the rationale for the prospective use of chemopreventive agents in translational studies.

Publication types

  • Research Support, N.I.H., Extramural
  • Review

MeSH terms

  • Angiogenesis Inhibitors / therapeutic use
  • Anticarcinogenic Agents / therapeutic use*
  • Cell Cycle / drug effects
  • Cell Survival / drug effects
  • Chemoprevention
  • Humans
  • Male
  • Neoplasm Invasiveness
  • Prostatic Neoplasms / blood supply
  • Prostatic Neoplasms / pathology
  • Prostatic Neoplasms / prevention & control*
  • Protein-Tyrosine Kinases / physiology
  • Receptors, Androgen / physiology
  • Signal Transduction


  • Angiogenesis Inhibitors
  • Anticarcinogenic Agents
  • Receptors, Androgen
  • Protein-Tyrosine Kinases