Delphinidin induced protective autophagy via mTOR pathway suppression and AMPK pathway activation in HER-2 positive

Jingyao Chen1, Yanfeng Zhu1, Weiwei Zhang1

  • 1Department of Public Health, Chengdu Medical College, 783 Xindu Avenue, Xindu, Chengdu, Sichuan, 610500, People's Republic of China.

BMC Cancer
|March 29, 2018
PubMed
Abstract

Insights

Delphinidin, an anthocyanin, inhibits growth and promotes apoptosis in HER-2 positive breast cancer cells by inducing autophagy. Suppressing autophagy enhances delphinidin

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Pharmacology

Background:

  • Anthocyanins exhibit anticancer properties.
  • This study focuses on delphinidin, a common anthocyanidin, and its role in autophagy within HER-2 positive breast cancer cells (MDA-MB-453 and BT474).

Purpose of the Study:

  • To investigate the biological activities of delphinidin related to autophagy in HER-2 positive breast cancer.
  • To analyze the effects of delphinidin on cancer cell proliferation and apoptosis.
  • To elucidate the autophagic mechanism and its influence on chemotherapy.

Main Methods:

  • Assessed delphinidin's impact on proliferation and apoptosis in MDA-MB-453 and BT474 cells.
  • Investigated the autophagic mechanism in delphinidin-treated cells.
  • Utilized autophagy inhibitors (3-MA and BA1) to evaluate the effects of autophagy inhibition.

Main Results:

  • Delphinidin demonstrated dose-dependent inhibition of proliferation, promotion of apoptosis, and induction of autophagy in cancer cells.
  • Inhibition of autophagy potentiated delphinidin's antiproliferative and pro-apoptotic effects.
  • Delphinidin induced autophagy through mTOR pathway suppression and AMPK pathway activation.

Conclusions:

  • Delphinidin induces apoptosis and autophagy in HER-2 positive breast cancer cells via mTOR and AMPK signaling.
  • Autophagy suppression enhances the anticancer efficacy of delphinidin.
  • Delphinidin shows potential as an anticancer agent for HER-2 positive breast cancer.

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