Delayed cytotoxic effects of methyl jasmonate and cis-jasmone induced apoptosis in prostate cancer cells

Cancer Invest. 2008 Nov;26(9):890-9. doi: 10.1080/07357900801975272.

Abstract

Advanced prostate cancer cells are typically hormone independent, resistant to apoptosis and do not respond to chemotherapeutic agents. The ability of methyl jasmonate (MJ) and cis-jasmone (CJ) to inhibit growth in hormone independent prostate cancer cell lines, PC-3 and DU-145, was evaluated. CJ and MJ inhibited cell growth, induced cell cycle arrest and apoptosis. Detailed studies with the PC-3 cell line revealed that 2 mM CJ or MJ treatment resulted in caspase 3 activation and Tumor Necrosis Factor Receptor 1 (TNFR1) activation, all hallmarks of apoptosis. These phytochemicals could be useful in the management of advanced prostate cancer.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acetates / pharmacology*
  • Antineoplastic Agents, Phytogenic / pharmacology*
  • Apoptosis*
  • Caspase 3 / biosynthesis
  • Cell Cycle / drug effects
  • Cell Line, Tumor
  • Cell Proliferation / drug effects
  • Cyclopentanes / pharmacology*
  • Humans
  • Male
  • Oxylipins / pharmacology*
  • Prostatic Neoplasms / metabolism*
  • Prostatic Neoplasms / pathology
  • Receptors, Tumor Necrosis Factor, Type I / biosynthesis

Substances

  • Acetates
  • Antineoplastic Agents, Phytogenic
  • Cyclopentanes
  • Oxylipins
  • Receptors, Tumor Necrosis Factor, Type I
  • methyl jasmonate
  • Caspase 3
  • jasmone