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Arctigenin induces apoptosis in colon cancer cells through ROS/p38MAPK pathway

Qing-chun Li1, Yun Liang, Yuan Tian

  • 1Department of Gastrointestinal Surgery, China-Japan Union Hospital of Jilin University, Changchun, Jilin, 130033, China.

Journal of B.U.ON. : Official Journal of the Balkan Union of Oncology
|April 11, 2016
PubMed
Abstract

Insights

Arctigenin, a plant lignin, effectively inhibits human colon cancer cell growth by inducing apoptosis. This occurs through the regulation of reactive oxygen species (ROS) and p38 mitogen-activated protein kinase (MAPK) pathways.

Area of Science:

  • Oncology
  • Molecular Biology
  • Pharmacology

Background:

  • Colon cancer remains a significant global health challenge.
  • Natural compounds are being investigated for their therapeutic potential.
  • Arctigenin is a plant-derived lignin with potential biological activities.

Purpose of the Study:

  • To evaluate the antiproliferative effects of arctigenin on the human colon cancer cell line HT-29.
  • To elucidate the signaling mechanisms underlying arctigenin's anti-cancer effects.

Main Methods:

  • Cell viability assessed using MTT and LDH assays.
  • Cell cycle arrest and apoptosis quantified by flow cytometry.
  • Caspase-9 and -3 activities, reactive oxygen species (ROS), and p38 mitogen-activated protein kinase (MAPK) levels were analyzed.

Main Results:

  • Arctigenin demonstrated significant, dose-dependent inhibition of HT-29 cell growth.
  • Arctigenin treatment led to G2/M phase cell cycle arrest and increased apoptosis.
  • Activation of caspase-9, caspase-3, ROS production, and p38 MAPK indicated intrinsic apoptotic pathway involvement.

Conclusions:

  • Arctigenin induces apoptosis in HT-29 colon cancer cells.
  • The mechanism involves the regulation of ROS and p38 MAPK signaling pathways.

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