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2-(3-methoxyphenyl)-6,7-methylenedioxoquinolin-4-one (MMEQ) is a novel synthesizedcompound, and this study investigated the effects of MMEQ on molecular signalpathways of the induction of apoptosis in TSGH8301 human bladder cancer cells.The studies included examining the effects of morphological changes by contrast-phasemicroscope, the percentage of viable cells, cell cycle distribution mitochondriamembrane potential (ΔΨm), ROS and caspase activities were examined by flow cytometry,apoptotic cells were examined by DAPI staining and the changes of associated apoptosisproteins levels were examined by Western blotting. Release of apoptotic factorsfrom mitochondria was examined by confocal laser microscope. Our results showedthat MMEQ caused morphological changes and inhibited the cell growth of TSGH8301cells in a time- and dose-dependent manner. MMEQ induced G2/M arrest through thepromotion of chk1, chk2 and cdc25c in TSGH8301 cells. MMEQ caused a marked increasein the percentage of DNA damage and apoptosis as characterized by DAPI and DNAfragmentation. The specific inhibitors of caspase-8, -9, and -3 blocked MMEQ-inducedgrowth inhibition action. A remarkable loss of ΔΨm and increase in ROS productionwere observed after a 24-h treatment. MMEQ promoted the levels of caspase-3, caspase-8,caspase-9, Bax, Bcl-xs, decreased the levels of Bcl-2 and Bid and then led todysfunction of ΔΨm, following the releases of cytochrome c, AIF and Endo G frommitochondria to cytosol and nuclei, and finally caused cell apoptosis. In conclusions,these molecular mechanisms provide insight into MMEQ-caused growth inhibition,G2/M arrest and apoptotic cell death in TSGH8301 cells.

international journal of oncology

A novel synthetic 2-(3-methoxyphenyl)-6,7-methylenedioxoquinolin-4-one arrests the G2/M phase arrest via Cdc25c and induces apoptosis through caspase- and mitochondria-dependent pathways in TSGH8301 human bladder cancer cells