Long noncoding RNA LINC00336 inhibits ferroptosis in lung cancer by functioning as a competing endogenous RNA | |
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 |
2019-11-01 | |
卷号 | 26期号:11页码:2329-2343 |
ISSN号 | 1350-9047 |
DOI | 10.1038/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. |
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关键词 | LYMPHOID-SPECIFIC HELICASE ; METHYLATION PATTERNS ; DNA METHYLATION ; CELL-DEATH ; LSH ; EXPRESSION ; HUR ; PROLIFERATION ; LOCALIZATION ; METASTASIS |
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 |
内容类型 | 期刊论文 |
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. |
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