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Published on: May 30, 2012

Apigenin Induces Apoptosis through a Mitochondria/Caspase-Pathway in Human Breast Cancer MDA-MB-453 Cells

Eun Jeong Choi1, Gun-Hee Kim

  • 1Plant Resources Research Institute, Duksung Women's University, 419 Ssangmun-dong, Tobong-ku, Seoul 132-714, South Korea.

Journal of Clinical Biochemistry and Nutrition
|May 12, 2009
PubMed

Insights

Apigenin, a potential anticancer drug, triggers programmed cell death (apoptosis) in breast cancer cells. It activates both intrinsic and extrinsic cell death pathways by cleaving key caspases.

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Cancer Research

Background:

  • Apigenin is investigated as a non-cytotoxic anticancer agent.
  • Understanding its mechanism in apoptosis is crucial for drug development.

Purpose of the Study:

  • To elucidate the role of the caspase cascade in apigenin-induced apoptosis.
  • To determine if apigenin activates both intrinsic and extrinsic apoptotic pathways.

Main Methods:

  • Treatment of MDA-MB-453 human breast cancer cells with varying concentrations of apigenin.
  • Assessment of cell proliferation inhibition and apoptosis induction.
  • Analysis of caspase cleavage and cytochrome c release.

Main Results:

  • Apigenin inhibited breast cancer cell proliferation in a dose- and time-dependent manner.
  • Apigenin induced apoptosis, cytochrome c release, and cleavage of caspase-9.
  • Apigenin activated caspase-3, leading to the cleavage of caspases-6, -7, and -8, indicating activation of both intrinsic and extrinsic pathways.

Conclusions:

  • Apigenin-induced apoptosis in breast cancer cells involves the caspase cascade.
  • Apigenin activates both the intrinsic and extrinsic apoptotic pathways, supporting its potential as an anticancer therapeutic.
Keywords:
apigeninapoptosiscaspases cascadehuman breast cancer MDA-MB-453 cells

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