Pseudolaric acid B induces apoptosis,senescence,and mitotic arrest in human breast cancer MCF-7
Pseudolaric acid B induces apoptosis,senescence,and mitotic arrest in human breast cancer MCF-7作者机构：Department of Clinical and Biomedical SciencesShowa Pharmaceutical University Tokyo 194-8543Japan China-Japan Research Institute of Medical Pharmaceutical SciencesShenyang Pharmaceutical UniversityShenyang 110016China
出 版 物：《Acta Pharmacologica Sinica》 (中国药理学报(英文版))
年 卷 期：2007年第28卷第12期
页 面：1975-1983页
核心收录：
学科分类：1007[医学-药学(可授医学、理学学位)] 1002[医学-临床医学] 100214[医学-肿瘤学] 10[医学]
主 题：apoptosis senescence mitotic arrest human breast cancer MCF-7 pseudolaric acid B
摘 要：Aim:The aim of the present study was to investigate the inhibitory effect ofpseudolaric acid B （PAB） on human breast cancer MCF-7 ***:3-（4,5-dimethylthiazol-2-yl）-2,5-diphenyltetrazolium bromide analysis,morphologicalchanges,acridine orange staining,and agarose gel electrophoresis were appliedto detect *** percentage of apoptotic and necrotic cells was calcu-lated by the lactate dehydrogenase activity-based cytotoxicity assay;senescenceassociated （SA）-β-galactosidase activity was detected to evaluate senescence;flow cytometric analysis of propidium iodide staining was carried out to investi-gate the distribution of cell cycle,and the protein expression was examined byWestern blot ***:During apoptosis,the half maximal inhibitoryconcentration IC50was 3.4 and 1.35 μmol/L at 36 and 48 h after PAB treatment,*** MCF-7 cells exposed to PAB showed typical characteristics ofapoptosis,including the morphological changes and DNA ***-7 cells treated with 4 μmol/L PAB for 36 h underwent apoptosis,but *** apoptosis induced by PAB was independent of the death *** senescent cells became larger and flatter,and the SA-β-galactosi-dase staining was *** induced obvious mitotic arrest and it precededapoptosis and *** expressions of p21 and p53 was upregulated withPAB treatment,and cyclin B 1 was upregulated and transported from the cyto-plasm to nuclei,and sustained stable ***:PAB induced mitoticarrest in the MCF-7 cells and inhibited proliferation through apoptosis *** apoptosis was independent of the death receptor pathway.
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