Antitumor properties of Coenzyme Q0 against human ovarian carcinoma cells via induction of ROS-mediated apoptosis and cytoprotective autophagy.
作者： You-Cheng Hseu , Tai-Jung Tsai , Mallikarjuna Korivi , Jer-Yuh Liu , Hui-Jye Chen
DOI: 10.1038/S41598-017-08659-7
关键词:
摘要: Coenzyme Q0 (CoQ0, 2,3-dimethoxy-5-methyl-1,4-benzoquinone) has been reported to exert anticancer properties against human breast/lung cancer cells. This study investigated the in vitro and vivo of CoQ0 on ovarian carcinoma (SKOV-3) cells xenografted nude mice, revealed underlying molecular mechanism. induced G2/M arrest through downregulation cyclin B1/A CDK1/K2 expressions. CoQ0-induced autophagy as a survival mechanism was evidenced by increased accumulation LC3-II, GFP-LC3 puncta, AVOs formation Beclin-1/Bcl-2 dysregulation. Increased TUNEL-positive Annexin-V/PI stained indicated late apoptosis. Both mitochondrial (caspase-3, PARP Bax/Bcl-2 dysregulation) ER stress (caspase-12 Hsp70) signals are involved execution Interestingly, apoptosis/autophagy is associated with suppression HER-2/neu PI3K/AKT signalling cascades. triggered intracellular ROS production, whereas antioxidant N-acetylcysteine prevented apoptosis, but not autophagy. Inhibition apoptosis Z-VAD-FMK suppressed (diminished LC3-II/AVOs), indicates led evoke Contrary, inhibition 3-MA/CQ potentiated (increased DNA fragmentation/PARP cleavage). Furthermore, treatment SKOV-3 mice reduced tumor incidence burden. Histopathological analyses confirmed that modulated progression induction. Our findings emphasize ROS-mediated cytoprotective
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