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Long noncoding RNA LINC00336 inhibits ferroptosis in lung cancer by functioning as a competing endogenous RNA

文献类型：期刊论文

作者Wang, Min1,2,6; Mao, Chao1,2; Ouyang, Lianlian1,2,5; Liu, Yating1,2; Lai, Weiwei1,2; Liu, Na1,2; Shi, Ying1,2; Chen, Ling1,2; Xiao, Desheng4; Yu, Fenglei3
刊名CELL DEATH AND DIFFERENTIATION
出版日期2019-11-01
卷号26期号:11页码:2329-2343
ISSN号1350-9047
DOI10.1038/s41418-019-0304-y
通讯作者Tao, Yongguang(taoyong@csu.edu.cn) ; Zhang, Bin(coolzhangbin22@163.com)
英文摘要The regulatory loop between long noncoding RNAs (lncRNAs) and microRNAs has a dynamic role in transcriptional and translational regulation, and is involved in cancer. However, the regulatory circuitry between lncRNAs and microRNAs in tumorigenesis remains elusive. Here we demonstrate that a nuclear lncRNA LINC00336 is upregulated in lung cancer and functions as an oncogene by acting as a competing endogenous RNA (ceRNAs). LINC00336 bound RNA-binding protein ELAVL1 (ELAV-like RNA-binding protein 1) using nucleotides 1901-2107 of LINC00336 and the RRM interaction domain and key amino acids (aa) of ELAVL1 (aa 101-213), inhibiting ferroptosis. Moreover, ELAVL1 increased LINC00336 expression by stabilizing its posttranscriptional level, whereas LSH (lymphoid-specific helicase) increased ELAVL1 expression through the p53 signaling pathway, further supporting the hypothesis that LSH promotes LINC00336 expression. Interestingly, LINC00336 served as an endogenous sponge of microRNA 6852 (MIR6852) to regulate the expression of cystathionine-beta-synthase (CBS), a surrogate marker of ferroptosis. Finally, we found that MIR6852 inhibited cell growth by promoting ferroptosis. These data show that the network of lncRNA and ceRNA has an important role in tumorigenesis and ferroptosis.
WOS关键词LYMPHOID-SPECIFIC HELICASE ; METHYLATION PATTERNS ; DNA METHYLATION ; CELL-DEATH ; LSH ; EXPRESSION ; HUR ; PROLIFERATION ; LOCALIZATION ; METASTASIS
资助项目National Natural Science Foundation of China[81672787] ; National Natural Science Foundation of China[81772496] ; National Natural Science Foundation of China[81772927] ; National Natural Science Foundation of China[81672991] ; National Natural Science Foundation of China[81874139] ; National Natural Science Foundation of China[81672307] ; National Basic Research Program of China[2015CB553903] ; Fundamental Research Funds for the Central Universities[2018zzts829] ; Fundamental Research Funds for the Central Universities[2015zzts099]
WOS研究方向Biochemistry & Molecular Biology ; Cell Biology
语种英语
出版者NATURE PUBLISHING GROUP
WOS记录号WOS:000489164900011
源URL[http://119.78.100.183/handle/2S10ELR8/282705]  
专题中国科学院上海药物研究所
通讯作者Tao, Yongguang; Zhang, Bin
作者单位1.Cent S Univ, Xiangya Hosp, Dept Pathol, Key Lab Carcinogenesis & Canc Invas,Minist Educ, Changsha 410078, Hunan, Peoples R China
2.Cent S Univ, NHC Key Lab Carcinogenesis, Canc Res Inst, Changsha 410078, Hunan, Peoples R China
3.Cent S Univ, Xiangya Hosp 2, Dept Thorac Surg, Changsha 410011, Hunan, Peoples R China
4.Cent S Univ, Xiangya Hosp, Dept Pathol, Changsha 410008, Hunan, Peoples R China
5.Cent S Univ, Xiangya Hosp, Inst Med Sci, Dept Oncol, Changsha 410008, Hunan, Peoples R China
6.Cent S Univ, Sch Basic Med, Dept Histol & Embryol, Changsha 410013, Hunan, Peoples R China
7.Yale Sch Med, Dept Pathol, New Haven, CT 06520 USA
8.Chinese Acad Sci, Shanghai Inst Mat Med, 555 Zu Chongzhi Rd,Zhangjiang Hitech Pk, Shanghai 201203, Peoples R China
推荐引用方式
GB/T 7714		 Wang, Min,Mao, Chao,Ouyang, Lianlian,et al. Long noncoding RNA LINC00336 inhibits ferroptosis in lung cancer by functioning as a competing endogenous RNA[J]. CELL DEATH AND DIFFERENTIATION,2019,26(11):2329-2343.
APA Wang, Min.,Mao, Chao.,Ouyang, Lianlian.,Liu, Yating.,Lai, Weiwei.,...&Zhang, Bin.(2019).Long noncoding RNA LINC00336 inhibits ferroptosis in lung cancer by functioning as a competing endogenous RNA.CELL DEATH AND DIFFERENTIATION,26(11),2329-2343.
MLA Wang, Min,et al."Long noncoding RNA LINC00336 inhibits ferroptosis in lung cancer by functioning as a competing endogenous RNA".CELL DEATH AND DIFFERENTIATION 26.11(2019):2329-2343.

入库方式： OAI收割

来源：上海药物研究所

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