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Ziliang Li,Boyu Qin,Xiaoguang Qi,Jingtao Mao,Dan Wu 대한약학회 2016 Archives of Pharmacal Research Vol.39 No.10
Isoalantolactone possessed various biological activities. However, whether it could treat breast cancer and its underlying mechanism remained largely unknown. This study was designed to evaluate the anticancer effects of isoalantolactoneonbreastcancerandexploredthemolecular mechanism.Twohumanbreastcancercelllines(MDA-MB231 and MCF-7) and one normal breast cellline (MCF-10A) were applied. Our data suggested that isoalantolactone decreased breast cancer cell viability in a dose-dependent manner, but showed almost no toxicity to MCF-10A cells. Theanticancereffectsofisoalantolactonewererelatedtothe overexpression of reactive oxygen species. Isoalantolactone significantly induced breast cancer cell apoptosis byactivating caspase cascade, cleaving poly (ADP-ribose) polymerase. Increase of Bax/Bcl-2 ratio, depolarization of mitochondrial membrane potential, release of cytochrome c from mitochondria to cytoplasm and cell cycle arrest at G2/ M phase were associated to the apoptosis induction. Additionally,isoalantolactoneincreasedtheproteinexpressionof p38 MAPK and JNK. The apoptosis-induction of isoalantolactone could be abrogated by co-treatment with SB203580 (inhibitor of p38 MAPK) or SP600125 (inhibitor of JNK). Furthermore, isoalantolactone induced breast cancer cells apoptosis in a caspase-independent pathway, which was downregulation of SIRT1. Therefore, isoalantolactone may serve as a chemotherapeutic agent for the treatment of human breast cancer.