[Delphinidin induces autophagy in HER-2+ breast cancer cells via inhibition of AKT/mTOR pathway].
Zhong Nan Da Xue Xue Bao Yi Xue Ban, 2017/3/28;42(3):264-270.
Chen J[1], Zhou J[1], Li F[1], Zhu Y[1], Zhang W[1], Yu X[1]
Affiliations
PMID: 28364098DOI: 10.11817/j.issn.1672-7347.2017.03.005
Abstract
objective: To explore the effect of delphinidin on breast cancer and the underlying mechanisms.
Methods: Human epidermal growth factor receptor-2 (HER-2) positive breast cancer cells MDA-MB-453 were treated by delphinidin. Proliferation of MDA-MB-453 cells was detected by CCK-8 after 48 h. TdT-mediated dUTP nick end labeling (TUNEL) assay and Western blot were used to explore apoptotic status for MDA-MB-453 cells. Fluorescence dot assay, immunofluorescence, and Western blot were used to identify autophagy in breast cancer cells.
Results: Delphinidin suppressed proliferation of MDA-MB-453 cells. Delphinidin increased the number of TUNEL positive cells. Delphinidin downregulated the expression of caspase-3 and caspase-9, while upregulated the expression of cleaved caspase-3 and cleaved caspase-9 in a dose-dependent manner. Delphinidin enhanced the number of GFP-LC3 punctate dots, LC3 immunofluorescence dots and the expression of LC3-II and ATG5. Delphinidin inhibited the expression of proteins in mTOR signaling pathway, including AKT, mTOR, eIF4E and p70s6k.
Conclusion: Delphinidin induced apoptosis and autophagy by inhibition of AKT/mTOR pathway in HER positive breast cancer cells.
MeSH terms
Anthocyanins; Apoptosis; Autophagy; Biomarkers, Tumor; Breast Neoplasms; Caspase 3; Caspase 9; Cell Line, Tumor; Cell Proliferation; Female; Humans; In Situ Nick-End Labeling; Neoplasm Proteins; Proto-Oncogene Proteins c-akt; Sincalide; TOR Serine-Threonine Kinases
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