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辅酶 Q 对人卵巢癌细胞的抗肿瘤作用通过诱导 ROS 介导的凋亡和细胞保护自噬。

Antitumor properties of Coenzyme Q against human ovarian carcinoma cells via induction of ROS-mediated apoptosis and cytoprotective autophagy.

机构信息

Department of Cosmeceutics, College of Biopharmaceutical and Food Sciences, China Medical University, Taichung, 40402, Taiwan.

Department of Health and Nutrition Biotechnology, Asia University, Taichung, 41354, Taiwan.

出版信息

Sci Rep. 2017 Aug 14;7(1):8062. doi: 10.1038/s41598-017-08659-7.

DOI:10.1038/s41598-017-08659-7
PMID:28808311
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5556069/
Abstract

Coenzyme Q (CoQ, 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 in vivo anticancer properties of CoQ on human ovarian carcinoma (SKOV-3) cells and xenografted nude mice, and revealed the underlying molecular mechanism. CoQ induced G/M arrest through downregulation of cyclin B1/A and CDK1/K2 expressions. CoQ-induced autophagy as a survival mechanism was evidenced by increased accumulation of LC3-II, GFP-LC3 puncta, AVOs formation and Beclin-1/Bcl-2 dysregulation. Increased TUNEL-positive cells and Annexin-V/PI stained cells indicated CoQ-induced late apoptosis. Both mitochondrial (caspase-3, PARP and Bax/Bcl-2 dysregulation) and ER stress (caspase-12 and Hsp70) signals are involved in execution of apoptosis. Interestingly, CoQ-induced apoptosis/autophagy is associated with suppression of HER-2/neu and PIK/AKT signalling cascades. CoQ triggered intracellular ROS production, whereas antioxidant N-acetylcysteine prevented CoQ-induced apoptosis, but not autophagy. Inhibition of apoptosis by Z-VAD-FMK suppressed CoQ-induced autophagy (diminished LC3-II/AVOs), indicates CoQ-induced apoptosis led to evoke autophagy. Contrary, inhibition of autophagy by 3-MA/CQ potentiated CoQ-induced apoptosis (increased DNA fragmentation/PARP cleavage). Furthermore, CoQ treatment to SKOV-3 xenografted nude mice reduced tumor incidence and burden. Histopathological analyses confirmed that CoQ modulated xenografted tumor progression by apoptosis induction. Our findings emphasize that CoQ triggered ROS-mediated apoptosis and cytoprotective autophagy.

摘要

辅酶 Q（CoQ，2,3-二甲氧基-5-甲基-1,4-苯醌）已被报道对人乳腺癌/肺癌细胞具有抗癌特性。本研究探讨了 CoQ 对人卵巢癌（SKOV-3）细胞和异种移植裸鼠的体外和体内抗癌特性，并揭示了潜在的分子机制。CoQ 通过下调细胞周期蛋白 B1/A 和 CDK1/K2 的表达诱导 G/M 期阻滞。CoQ 诱导的自噬作为一种存活机制，表现为 LC3-II、GFP-LC3 斑点、AVOs 形成和 Beclin-1/Bcl-2 失调的增加。增加的 TUNEL 阳性细胞和 Annexin-V/PI 染色细胞表明 CoQ 诱导晚期细胞凋亡。线粒体（caspase-3、PARP 和 Bax/Bcl-2 失调）和内质网应激（caspase-12 和 Hsp70）信号均参与细胞凋亡的执行。有趣的是，CoQ 诱导的细胞凋亡/自噬与 HER-2/neu 和 PIK/AKT 信号级联的抑制有关。CoQ 触发细胞内 ROS 的产生，而抗氧化剂 N-乙酰半胱氨酸可预防 CoQ 诱导的细胞凋亡，但不能预防自噬。凋亡抑制剂 Z-VAD-FMK 抑制 CoQ 诱导的自噬（减少 LC3-II/AVOs），表明 CoQ 诱导的凋亡导致自噬。相反，自噬抑制剂 3-MA/CQ 增强了 CoQ 诱导的细胞凋亡（增加 DNA 片段化/PARP 切割）。此外，CoQ 处理 SKOV-3 异种移植裸鼠可降低肿瘤发生率和肿瘤负担。组织病理学分析证实 CoQ 通过诱导细胞凋亡来调节异种移植肿瘤的进展。我们的研究结果强调，CoQ 触发了 ROS 介导的细胞凋亡和细胞保护自噬。

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