Affiliations 

  • 1 Scientific Research Department, Innoscience Research, Selangor, Malaysia
  • 2 Health Care Department for Women, Northwest Women's and Children's Hospital, Xi'an, China
  • 3 Department of Neurology, Xijing Hospital, Fourth Military Medical University (FMMU), Xi'an, China
  • 4 Department of Galactophore, Shandong Provincial Western Hospital, Jinan, China
J. Biochem. Mol. Toxicol., 2019 Apr;33(4):e22268.
PMID: 30431692 DOI: 10.1002/jbt.22268

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 on HER2/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.

* Title and MeSH Headings from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.