Inhibition of autophagy enhances Hydroquinone-induced TK6 cell death

被引:15
作者
Xu, Longmei [1 ,2 ]
Liu, Jiaxian [1 ,2 ]
Chen, Yuting [1 ,2 ]
Yun, Lin [1 ,2 ]
Chen, Shaoyun [1 ,2 ]
Zhou, Kairu [1 ,2 ]
Lai, Bei [1 ,2 ]
Song, Li [1 ,2 ]
Yang, Hui [1 ,2 ]
Liang, Hairong [1 ,2 ]
Tang, Huanwen [1 ,2 ]
机构
[1] Guangdong Med Univ, Sch Publ Hlth, PR-523808 Dongguan, Guangdong, Peoples R China
[2] Dongguan Key Lab Environm Med, PR-523808 Dongguan, Guangdong, Peoples R China
关键词
Autophagy; Hydroquinone; Apoptosis; 3-MA; CQ; PARP-1; DOWN-REGULATION; MONITORING AUTOPHAGY; SIGNALING PATHWAY; CIGARETTE-SMOKE; IN-VITRO; BENZENE; MECHANISM; TRANSFORMATION; GLIOBLASTOMA; GENOTOXICITY;
D O I
10.1016/j.tiv.2017.02.024
中图分类号
R99 [毒物学(毒理学)];
学科分类号
100405 ;
摘要
Hydroquinone (HQ), one of the metabolic products of benzene, is a carcinogen. It can induce apoptosis in lymphoma cells. However, whether HQcan induce autophagy and what roles autophagy plays in TK6 cells exposured to HQ remains unclear. In this study, we found that HQ could induce autophagy through techniques of qRT-PCR, Western blot, immunofluorescent assay of LC3 and transmission electron microscope. Furthermore, inhibiting autophagy using 3-methyladenine (3-MA) or chloroquine (CQ) significantly enhanced HQ-induced cell apoptosis, suggesting that autophagy may be a survival mechanism. Our study also showed that HQ activated PARP-1. Moreover, knockdown of PARP-1 strongly exhibited decreased autophagy related genes expression. In contrast, the absence of SIRT1 increased that. Altogether, our data provided evidence that HQ induced autophagy in TK6 cells and autophagy protected TK6 from HQ attack-induced injury in vitro, and the autophagy was partially mediated via activation of the PARP-1-SIRT1 signaling pathway. (C) 2017 Elsevier Ltd. All rights reserved.
引用
收藏
页码:123 / 132
页数:10
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