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LncRNA MT1DP Aggravates Cadmium-Induced Oxidative Stress by Repressing the Function of Nrf2 and is Dependent on Interaction with miR-365

文献类型：期刊论文

作者Gao, Ming1,2; Li, Changying3; Xu, Ming1,2; Liu, Yun1,4; Cong, Min3; Liu, Sijin1,2
刊名ADVANCED SCIENCE
出版日期2018-07-01
卷号5期号:7页码:9
关键词cadmium long non-coding RNA (lncRNA) miR-365 MT1DP Nrf2 oxidative stress
ISSN号2198-3844
DOI10.1002/advs.201800087
通讯作者Liu, Sijin(sjliu@rcees.ac.cn)
英文摘要Although cadmium (Cd)-induced hepatoxicity is well established, pronounced knowledge gaps remain existed regarding the inherent cellular signaling that dictates Cd toxicity. Specifically, the molecular basis for determining the equilibrium between prosurvival and proapoptotic signaling remains poorly understood. Thus, it is recently revealed that long non-coding RNA (lncRNA) MT1DP, a pseudogene in the metallothionein (MT) family, promoted Cd-induced cell death through activating the RhoC-CCN1/2-AKT pathway and modulating MT1H induction. Here, first the dependency of MT1DP induction on MTF1, an important transcriptional factor in driving the mRNA expression of MT1 members is defined. Additionally, a bridge molecule between MT1DP and nuclear factor erythroid 2-related factor 2 (Nrf2) is established: miR-365. Mechanistically, MT1DP induction under Cd stress decreases the nuclear factor erythroid 2-related factor 2 (Nrf2) level to evoke oxidative stress through the elevation of miR-365, which acted to repress the Nrf2 level via direct binding to its 3'UTR. In contrast to the competing endogenous RNA (ceRNA) mechanism, a new mechanism is proposed: MT1DP elevated the miR-365 level though stabilizing its RNA via direct binding. Collectively, the combined data demonstrate a crucial role of MT1DP in reducing the Nrf2-mediated protection of cells, and this is dependent on the interplay with miR-365. Hence, the study further expands the knowledge of inducible endogenous lncRNA in modulating oxidative stress.
WOS关键词LONG NONCODING RNA ; ERYTHROID-CELLS ; FACTOR-I ; TOXICITY ; LIVER ; GENE ; MECHANISMS ; EXPRESSION ; PATHWAYS ; EXPOSURE
资助项目Strategic Priority Research Program of the Chinese Academy of Sciences[XDB14000000] ; National Natural Science Foundation of China[21507154] ; National Natural Science Foundation of China[21425731] ; National Natural Science Foundation of China[21637004] ; National Natural Science Foundation of China[81570542] ; national 973 program[2014CB932000]
WOS研究方向Chemistry ; Science & Technology - Other Topics ; Materials Science
语种英语
WOS记录号WOS:000439842100017
出版者WILEY
资助机构Strategic Priority Research Program of the Chinese Academy of Sciences ; Strategic Priority Research Program of the Chinese Academy of Sciences ; Strategic Priority Research Program of the Chinese Academy of Sciences ; Strategic Priority Research Program of the Chinese Academy of Sciences ; Strategic Priority Research Program of the Chinese Academy of Sciences ; Strategic Priority Research Program of the Chinese Academy of Sciences ; Strategic Priority Research Program of the Chinese Academy of Sciences ; Strategic Priority Research Program of the Chinese Academy of Sciences ; Strategic Priority Research Program of the Chinese Academy of Sciences ; Strategic Priority Research Program of the Chinese Academy of Sciences ; Strategic Priority Research Program of the Chinese Academy of Sciences ; Strategic Priority Research Program of the Chinese Academy of Sciences ; Strategic Priority Research Program of the Chinese Academy of Sciences ; Strategic Priority Research Program of the Chinese Academy of Sciences ; Strategic Priority Research Program of the Chinese Academy of Sciences ; Strategic Priority Research Program of the Chinese Academy of Sciences ; National Natural Science Foundation of China ; National Natural Science Foundation of China ; National Natural Science Foundation of China ; National Natural Science Foundation of China ; National Natural Science Foundation of China ; National Natural Science Foundation of China ; National Natural Science Foundation of China ; National Natural Science Foundation of China ; National Natural Science Foundation of China ; National Natural Science Foundation of China ; National Natural Science Foundation of China ; National Natural Science Foundation of China ; National Natural Science Foundation of China ; National Natural Science Foundation of China ; National Natural Science Foundation of China ; National Natural Science Foundation of China ; national 973 program ; national 973 program ; national 973 program ; national 973 program ; national 973 program ; 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源URL[http://ir.hfcas.ac.cn:8080/handle/334002/37691]  
专题合肥物质科学研究院_技术生物与农业工程研究所
通讯作者Liu, Sijin
作者单位1.Chinese Acad Sci, Res Ctr Ecoenvironm Sci, State Key Lab Environm Chem & Ecotoxicol, Beijing 100085, Peoples R China
2.Univ Chinese Acad Sci, Coll Resources & Environm, Beijing 100049, Peoples R China
3.Capital Med Univ, Beijing Friendship Hosp, Liver Res Ctr, Beijing 100050, Peoples R China
4.Chinese Acad Sci & Anhui Prov, Hefei Inst Phys Sci, Key Lab Ion Beam Bioengn, Hefei 230031, Anhui, Peoples R China
推荐引用方式
GB/T 7714		 Gao, Ming,Li, Changying,Xu, Ming,et al. LncRNA MT1DP Aggravates Cadmium-Induced Oxidative Stress by Repressing the Function of Nrf2 and is Dependent on Interaction with miR-365[J]. ADVANCED SCIENCE,2018,5(7):9.
APA Gao, Ming,Li, Changying,Xu, Ming,Liu, Yun,Cong, Min,&Liu, Sijin.(2018).LncRNA MT1DP Aggravates Cadmium-Induced Oxidative Stress by Repressing the Function of Nrf2 and is Dependent on Interaction with miR-365.ADVANCED SCIENCE,5(7),9.
MLA Gao, Ming,et al."LncRNA MT1DP Aggravates Cadmium-Induced Oxidative Stress by Repressing the Function of Nrf2 and is Dependent on Interaction with miR-365".ADVANCED SCIENCE 5.7(2018):9.

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来源：合肥物质科学研究院

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