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Gut Bacterial Metabolite Urolithin A Decreases Actin Polymerization and Migration in Cancer Cells

Md Alauddin1, Toshiyuki Okumura1,2, Janet Rajaxavier1

  • 1Department of Women's Health, Eberhard Karls University of Tuebingen, Tübingen, 72076, Germany.

Molecular Nutrition & Food Research
|January 25, 2020
PubMed
Abstract

Insights

Urolithin A (UA), a metabolite from ellagic acid, disrupts cancer cell migration by affecting actin cytoskeleton regulation via Rac1 and PAK1. This dietary compound shows promise for cancer prevention and therapy.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Cancer Research

Background:

  • Urolithin A (UA) is a gut-derived metabolite of ellagic acid found in fruits and nuts.
  • Cell proliferation and migration are critical processes in cancer.
  • Actin cytoskeleton dynamics, regulated by Rac1 and PAK1, are essential for cell motility.

Purpose of the Study:

  • To investigate the effect of Urolithin A (UA) on the actin cytoskeleton in cancer cells.
  • To determine if UA modulates the activity of Rac1 and PAK1 pathways.
  • To explore the potential of UA in cancer prevention and therapy.

Main Methods:

  • Quantitative RT-PCR and immunoblotting were used to measure Rac1 and PAK1 levels.
  • Western blotting, immunofluorescence, and flow cytometry assessed the globular to filamentous actin ratio.
  • Cancer cell migration was evaluated using wound healing assays.

Main Results:

  • UA treatment (20 µm for 24 h) significantly reduced Rac1 and PAK1 transcript levels and activity.
  • UA induced actin depolymerization, decreasing the G:F-actin ratio.
  • UA treatment inhibited cancer cell migration, an effect mimicked by Rac1/PAK1 inhibition or knockdown.

Conclusions:

  • Urolithin A disrupts Rac1 and PAK1 activity, leading to actin depolymerization and reduced cancer cell migration.
  • Dietary Urolithin A demonstrates potential as a cancer preventive agent or adjuvant therapy.
  • Targeting Rac1 and PAK1 pathways with UA offers a promising strategy in cancer treatment.
Keywords:
PAK1Rac1actin polymerizationcarcinoma cells

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