LncRNA UCA1 attenuates autophagy-dependent cell death through blocking autophagic flux under arsenic stress
文献类型：期刊论文
| 作者 | Liu, Yun; Gao, Ming; Li, Changying; Xu, Ming; Liu, Sijin |
| 刊名 | TOXICOLOGY LETTERS
 |
| 出版日期 | 2018-03-01 |
| 卷号 | 284页码:195-204 |
| 关键词 | Arsenic toxicity Autophagy LncRNA UCA1 OSGIN1 |
| ISSN号 | 0378-4274 |
| 文献子类 | Article |
| 英文摘要 | Arsenic (As) is a naturally toxin which exists ubiquitously in foods and various environment media, incurring diverse toxicities and health problems. Previous studies have shown that oxidative stress, genotoxic damage and pro-apoptotic pathways are ascribed to As-associated detrimental effects. Meanwhile, epigenetic regulations (such as miRNAs and histone modifications) were also reported to contribute to As-induced adverse effects. Nonetheless, whether long non-coding RNAs (LncRNAs) are indispensable for the regulation of As-induced biological outcomes are nearly unknown. In this study, we identified that a lncRNA UCA1 was markedly induced by As treatment in human hepatocytes. Functional assessments revealed that UCA1 played a critical role in protecting hepatocytes from As-induced autophagy inhibition. Furthermore, through RNA-seq assay, oxidative stress induced growth inhibitor 1 (OSGIN1) was uncovered to be the most responsive target downstream of UCA1, and miR-184 acted as an intermediate for the regulation of UCA1 on the level of OSGIN1 through a competing endogenous RNAs (ceRNAs) mechanism. Further mechanistic investigations demonstrated that UCA1/OSGIN1 signaling contributed to As-induced autophagic flux blockage through activating mTOR/p70S6 K cascade, resulting in compromised cell death. Collectively, our study deciphered a lncRNA-dictated molecular mechanism responsible for As toxicity: UCA1 leads a protective role against As-induced cell death through blocking autophagic flux. |
| 源URL | [http://ir.rcees.ac.cn/handle/311016/40975]  |
| 专题 | 生态环境研究中心_环境化学与生态毒理学国家重点实验室 |
| 推荐引用方式 GB/T 7714 | Liu, Yun,Gao, Ming,Li, Changying,et al. LncRNA UCA1 attenuates autophagy-dependent cell death through blocking autophagic flux under arsenic stress[J]. TOXICOLOGY LETTERS,2018,284:195-204. |
| APA | Liu, Yun,Gao, Ming,Li, Changying,Xu, Ming,&Liu, Sijin.(2018).LncRNA UCA1 attenuates autophagy-dependent cell death through blocking autophagic flux under arsenic stress.TOXICOLOGY LETTERS,284,195-204. |
| MLA | Liu, Yun,et al."LncRNA UCA1 attenuates autophagy-dependent cell death through blocking autophagic flux under arsenic stress".TOXICOLOGY LETTERS 284(2018):195-204. |
入库方式： OAI收割
来源：生态环境研究中心
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