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Enterolactone induces apoptosis in human prostate carcinoma LNCaP cells via a mitochondrial-mediated,

Li-Hua Chen1, Jing Fang, Huaixing Li

  • 1Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, and Graduate School of the Chinese Academy of Sciences, Shanghai, China.

Molecular Cancer Therapeutics
|September 19, 2007
PubMed

Insights

Enterolactone, a metabolite of plant lignans, selectively kills prostate cancer cells by inducing apoptosis. This process involves mitochondrial dysfunction and caspase activation, suggesting its potential as a cancer preventive agent.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Enterolactone is a mammalian lignan metabolite derived from plant lignans.
  • Enterolactone has demonstrated inhibitory effects on prostate cancer growth and development.
  • The precise mechanisms underlying enterolactone's anticancer activity remain largely unelucidated.

Purpose of the Study:

  • To investigate the mechanistic basis of enterolactone's selective suppression of prostate cancer cell growth.
  • To elucidate the role of apoptosis in enterolactone's anticancer effects.
  • To identify key molecular players involved in enterolactone-induced apoptosis.

Main Methods:

  • Utilized LNCaP prostate cancer cells to assess enterolactone's effects.
  • Quantified mitochondrial membrane potential and cytochrome c release.
  • Analyzed procaspase-3 and poly(ADP-ribose)-polymerase (PARP) cleavage.
  • Employed a pan-caspase inhibitor (z-VAD-fmk) to confirm caspase dependence.
  • Investigated the involvement of signaling pathways including Akt, GSK-3beta, MDM2, and p53.

Main Results:

  • Enterolactone selectively inhibited the growth of LNCaP prostate cancer cells.
  • Enterolactone triggered apoptosis, evidenced by dose-dependent mitochondrial membrane potential loss and cytochrome c release.
  • Cleavage of procaspase-3 and PARP confirmed apoptosis induction.
  • Enterolactone-mediated apoptosis was caspase-dependent.
  • Akt, GSK-3beta, MDM2, and p53 were implicated in the apoptotic process.

Conclusions:

  • Enterolactone induces apoptosis in prostate cancer cells via mitochondrial pathways and caspase activation.
  • The study identifies key molecular mediators of enterolactone's action.
  • Enterolactone shows promise as a chemopreventive agent for prostate cancer, warranting further investigation.

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