title: [Delphinidin induces autophagy in HER-2+ breast cancer cells via inhibition of AKT/mTOR pathway].
abstract: 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.
authors.affiliation: Department of Public Health, Chengdu Medical College, Chengdu 610500, China.
authors.forename: Jingyao
authors.initials: J
authors.lastname: Chen
authors.affiliation: Department of Public Health, Chengdu Medical College, Chengdu 610500, China.
authors.forename: Jie
authors.initials: J
authors.lastname: Zhou
authors.affiliation: Department of Public Health, Chengdu Medical College, Chengdu 610500, China.
authors.forename: Fei
authors.initials: F
authors.lastname: Li
authors.affiliation: Department of Public Health, Chengdu Medical College, Chengdu 610500, China.
authors.forename: Yanfeng
authors.initials: Y
authors.lastname: Zhu
authors.affiliation: Department of Public Health, Chengdu Medical College, Chengdu 610500, China.
authors.forename: Weiwei
authors.initials: W
authors.lastname: Zhang
authors.affiliation: Department of Public Health, Chengdu Medical College, Chengdu 610500, China.
authors.forename: Xiaoping
authors.initials: X
authors.lastname: Yu
mesh_terms: D000872:Anthocyanins / Q000494:pharmacology*; D017209:Apoptosis; D001343:Autophagy / Q000187:drug effects*; D014408:Biomarkers, Tumor / Q000378:metabolism; D001943:Breast Neoplasms / Q000737:chemistry / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D053148:Caspase 3 / Q000378:metabolism; D053453:Caspase 9 / Q000378:metabolism; D045744:Cell Line, Tumor; D049109:Cell Proliferation / Q000187:drug effects*; D005260:Female; D006801:Humans; D020287:In Situ Nick-End Labeling; D009363:Neoplasm Proteins / Q000037:antagonists & inhibitors; D051057:Proto-Oncogene Proteins c-akt / Q000037:antagonists & inhibitors*; D012844:Sincalide / Q000378:metabolism; D058570:TOR Serine-Threonine Kinases / Q000037:antagonists & inhibitors*
chemical_list: D000872:Anthocyanins; D014408:Biomarkers, Tumor; D009363:Neoplasm Proteins; C546842:MTOR protein, human; D051057:Proto-Oncogene Proteins c-akt; D058570:TOR Serine-Threonine Kinases; D053148:Caspase 3; D053453:Caspase 9; C017185:delphinidin; D012844:Sincalide