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Updated: Jun 25, 2026

An Orthotopic Murine Model of Human Prostate Cancer Metastasis
06:48

An Orthotopic Murine Model of Human Prostate Cancer Metastasis

Published on: September 18, 2013

Enterolactone inhibits insulin-like growth factor-1 receptor signaling in human prostatic carcinoma PC-3 cells

Li-Hua Chen1, Jing Fang, Zhijian Sun

  • 1Key Laboratory of Nutrition and Metabolism, Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Graduate School of Chinese Academy of Sciences, Shanghai 200031, China.

The Journal of Nutrition
|February 13, 2009
PubMed

Insights

Enterolactone, a prostate cancer inhibitor, suppresses cancer cell growth and migration by blocking the insulin-like growth factor-1 (IGF-1)/IGF-1 receptor (IGF-1R) pathway. This study reveals a key mechanism for enterolactone's anticancer effects.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Pharmacology

Background:

  • Enterolactone (ENL), a plant lignan metabolite, exhibits anticancer properties against prostate cancer.
  • The precise molecular mechanisms underlying ENL's effects are not fully understood.
  • Insulin-like growth factor-1 receptor (IGF-1R) signaling is crucial for prostate cancer progression.

Purpose of the Study:

  • To investigate if enterolactone's growth inhibitory effects are mediated by the IGF-1/IGF-1R signaling pathway.
  • To explore the impact of enterolactone on key downstream signaling molecules in prostate cancer cells.

Main Methods:

  • PC-3 prostate cancer cells were treated with nutritionally relevant concentrations of enterolactone.
  • Western blotting was used to assess the phosphorylation of IGF-1R, AKT, and extracellular signal-regulated kinase (ERK).
  • Cyclin D1 expression, cell proliferation, and migration were evaluated. IGF-1R knockdown was performed using siRNA.

Main Results:

  • Enterolactone inhibited IGF-1-induced activation of IGF-1R, AKT, and ERK signaling pathways.
  • Enterolactone decreased the phosphorylation of downstream targets of AKT, including p70S6K1 and GSK-3β.
  • Enterolactone reduced cyclin D1 expression, inhibited PC-3 cell proliferation and migration.
  • Knockdown of IGF-1R abolished the effects of enterolactone on cell proliferation, indicating pathway dependency.

Conclusions:

  • Enterolactone suppresses prostate cancer cell proliferation and migration, at least partially, via inhibition of the IGF-1/IGF-1R signaling pathway.
  • This study elucidates novel molecular mechanisms of enterolactone's anticancer activity.
  • Findings provide a basis for exploring enterolactone as a potential therapeutic agent for prostate cancer.

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