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

Authors :
Jingyao Chen
Yanfeng Zhu
Weiwei Zhang
Xiaoli Peng
Jie Zhou
Fei Li
Bin Han
Xin Liu
Yu Ou
Xiaoping Yu
Source :
BMC Cancer, Vol 18, Iss 1, Pp 1-13 (2018)
Publication Year :
2018
Publisher :
BMC, 2018.

Abstract

Abstract Background We have previously demonstrated the anticancer effect of anthocyanins. In this study, we explored the biological activities of delphinidin, the most common of the anthocyanidin monomers, that were related to autophagy in HER-2 positive breast cancer MDA-MB-453 and BT474 cells. Methods The effects of various doses of delphinidin on the proliferation and apoptosis of MDA-MB-453 and BT474 cells were analysed. Autophagy was identified as a critical factor that influenced chemotherapy, and the autophagic mechanism in delphinidin-treated cells was investigated. The autophagy inhibitors, 3-MA and BA1, were used to analyse the effects of autophagy inhibition. Results Delphinidin inhibited proliferation, promoted apoptosis, and induced autophagy in MDA-MB-453 and BT474 cells in a dose-dependent manner. The inhibition of autophagy enhanced the delphinidin-induced apoptosis and antiproliferative effect in both HER-2 positive breast cancer cells. In addition, delphinidin induced autophagy via suppression of the mTOR signalling pathway and activation of the AMPK signalling pathway in HER-2 positive breast cancer cells. Conclusions Collectively, the results showed that delphinidin induced apoptosis and autophagy in HER-2 positive breast cancer cells and that autophagy was induced via the mTOR and AMPK signalling pathways. The suppression of autophagy promoted the anticancer effects of delphinidin.

Details

Language :
English
ISSN :
14712407
Volume :
18
Issue :
1
Database :
Directory of Open Access Journals
Journal :
BMC Cancer
Publication Type :
Academic Journal
Accession number :
edsdoj.6558057c9b0439da4d968763eb51a57
Document Type :
article
Full Text :
https://doi.org/10.1186/s12885-018-4231-y