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

Y.-M. Yang, Y. Yang, W.-W. Dai, X.-M. Li, J.-Q. Ma, L.-P. Tang

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

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• Pharmacology

OBJECTIVE: Genistein, a major isoflavone found in soybeans, exhibits anti-cancer activity. Endoplasmic reticulum (ER) stress is known to be implicated in apoptosis induced by anti-cancer drugs. This study aimed to characterize the role of ER stress in genistein-induced apoptosis in cervical cancer.

MATERIALS AND METHODS: HeLa cells were treated with genistein or/and 4-phenylbutyric acid. Cell viability and apoptosis were evaluated by MTT assay and flow cytometry. Protein levels were detected by Western blot analysis.

RESULTS: Genistein suppressed the viability of HeLa cells in a dose dependent manner. In addition, genistein caused apoptosis in HeLa cells in a dose dependent manner. Genistein triggered ER stress in HeLa cells, as indicated by the upregulation of glucose-regulated protein 78 (GRP78) and CHOP expression. Furthermore, ER stress inhibitor 4-phenylbutyric acid alleviated genistein-induced apoptosis and ER stress in HeLa cells.

CONCLUSIONS: Our results suggest that ER stress contributes to genistein-induced apoptosis in cervical cancer cells, and genistein is a promising agent for cervical cancer therapy.

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