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Abstract Title:

Fisetin induces apoptosis in breast cancer MDA-MB-453 cells through degradation of HER2/neu and via the PI3K/Akt pathway.

Abstract Source:

J Biochem Mol Toxicol. 2018 Nov 15:e22268. Epub 2018 Nov 15. PMID: 30431692

Abstract Author(s):

Gang Guo, Wenjie Zhang, Minyan Dang, Mingzhu Yan, Zheng Chen

Article Affiliation:

Gang Guo

Abstract:

Overexpression of human epidermal growth factor receptor 2 (HER2) is observed in breast cancer. The major snag faced by the human population is the development of chemoresistance to HER2 inhibitors by advanced stage breast cancer cells. Moreover, recent researchers focussed on fisetin as an antiproliferative and chemotherapeutic agent. Therefore, this study was intended to analyze the effects of fisetin onHER2/neu-overexpressing breast cancer cell lines. Our results depicted that fisetin induced apoptosis of these cells by various mechanisms, such as inactivation of the receptor, induction of proteasomal degradation, decreasing its half-life, decreasing enolase phosphorylation, and alteration of phosphatidylinositol 3-kinase/Akt signaling.

Study Type : In Vitro Study

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