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Genistein-induced apoptosis is mediated by endoplasmic reticulum stress in cervical cancer cells

Y-M Yang1, Y Yang, W-W Dai

  • 1Cancer Research Institute, Harbin Medical University, Harbin, China. hanzhigang@medmail.com.cn.

European Review for Medical and Pharmacological Sciences
|July 29, 2016
PubMed
Abstract

Insights

Genistein, a soy isoflavone, induces apoptosis in cervical cancer cells by triggering endoplasmic reticulum (ER) stress. This ER stress response is crucial for genistein

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Oncology

Background:

  • Genistein, a soy-derived isoflavone, demonstrates anti-cancer properties.
  • Endoplasmic reticulum (ER) stress is a known factor in drug-induced apoptosis.

Purpose of the Study:

  • To investigate the role of ER stress in genistein-induced apoptosis in cervical cancer cells.

Main Methods:

  • HeLa cervical cancer cells were treated with genistein and/or 4-phenylbutyric acid (an ER stress inhibitor).
  • Cell viability was assessed using MTT assay.
  • Apoptosis and protein expression (GRP78, CHOP) were analyzed via flow cytometry and Western blot.

Main Results:

  • Genistein reduced HeLa cell viability and induced apoptosis in a dose-dependent manner.
  • Genistein treatment upregulated ER stress markers glucose-regulated protein 78 (GRP78) and CHOP.
  • The ER stress inhibitor 4-phenylbutyric acid attenuated genistein-induced apoptosis and ER stress.

Conclusions:

  • ER stress plays a significant role in genistein-induced apoptosis in cervical cancer.
  • Genistein shows potential as a therapeutic agent for cervical cancer.

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