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A G3BP1-Interacting lncRNA Promotes Ferroptosis and Apoptosis in Cancer via Nuclear Sequestration of p53

文献类型：期刊论文

作者Mao, Chao4,5; Wang, Xiang6; Liu, Yating4,5; Wang, Min4,5; Bin Yan4,5; Jiang, Yiqun4,5,6; Shi, Ying4,5; Shen, Yi8; Liu, Xiaoli4,5; Lai, Weiwei4,5
刊名CANCER RESEARCH
出版日期2018-07-01
卷号78期号:13页码:3484-3496
ISSN号0008-5472
DOI10.1158/0008-5472.CAN-17-3454
文献子类Article
英文摘要Long noncoding RNAs (lncRNA) have been associated with various types of cancer; however, the precise role of many lncRNAs in tumorigenesis remains elusive. Here we demonstrate that the cytosolic lncRNA P53RRA is downregulated in cancers and functions as a tumor suppressor by inhibiting cancer progression. Chromatin remodeling proteins LSH and Cfp1 silenced or increased P53RRA expression, respectively. P53RRA bound Ras GTPase-activating protein-binding protein 1 (G3BP1) using nucleotides 1 and 871 of P53RRA and the RRM interaction domain of G3BP1 (aa 177-466). The cytosolic P53RRA-G3BP1 interaction displaced p53 from a G3BP1 complex, resulting in greater p53 retention in the nucleus, which led to cell-cycle arrest, apoptosis, and ferroptosis. P53RRA promoted ferroptosis and apoptosis by affecting transcription of several metabolic genes. Low P53RRA expression significantly correlated with poor survival in patients with breast and lung cancers harboring wild-type p53. These data show that lncRNAs can directly interact with the functional domain of signaling proteins in the cytoplasm, thus regulating p53 modulators to suppress cancer progression. Significance: A cytosolic lncRNA functions as a tumor suppressor by activating the p53 pathway. (C) 2018 AACR.
WOS关键词LYMPHOID-SPECIFIC HELICASE ; EMBRYONIC STEM-CELLS ; LONG NONCODING RNAS ; GENE-EXPRESSION ; BREAST-CANCER ; DNA-DAMAGE ; TRANSCRIPTION ; ACTIVATION ; PATHWAY ; STRESS
资助项目Frederick National Laboratory for Cancer Research, NIH[HHSN261200800001E] ; Intramural Research Program of NIH, Frederick National Lab, Center for Cancer Research[00000000] ; National Basic Research Program of China[2015CB553903] ; National Natural Science Foundation of China[81672787] ; National Natural Science Foundation of China[81372427] ; National Natural Science Foundation of China[81672307] ; National Natural Science Foundation of China[81672991] ; National Natural Science Foundation of China[81302354] ; National Natural Science Foundation of China[81422051] ; National Natural Science Foundation of China[81472593] ; Fundamental Research Funds for the Central Universities[2015zzts099]
WOS研究方向Oncology
语种英语
WOS记录号WOS:000437214300008
出版者AMER ASSOC CANCER RESEARCH
源URL[http://119.78.100.183/handle/2S10ELR8/279683]  
专题分析化学研究室
通讯作者Tao, Yongguang
作者单位1.Chinese Acad Sci, Shanghai Inst Mat Med, Zhangjiang Hitech Pk, Shanghai, Peoples R China;
2.Cipher Gene Beijing Co Ltd, Beijing, Peoples R China;
3.NCI, Mouse Canc Genet Program, Basic Sci Program, Leidos Biomed Res Inc,Frederick Natl Lab Canc Res, Frederick, MD 21701 USA
4.Cent S Univ, Xiangya Hosp, Minist Educ, Key Lab Carcinogenesis & Canc Invas, Changsha, Hunan, Peoples R China;
5.Cent S Univ, Key Lab Carcinogenesis, Minist Hlth, Canc Res Inst, Changsha, Hunan, Peoples R China;
6.Cent S Univ, Dept Thorac Surg, Xiangya Hosp 2, Changsha, Hunan, Peoples R China;
7.Cent S Univ, Xiangya Hosp, Dept Pathol, Changsha, Hunan, Peoples R China;
8.Univ Hawaii, Ctr Canc, Canc Epidemiol Program, Honolulu, HI 96822 USA;
9.Cent S Univ, Sch Pharmaceut Sci, Dept Pharmacol, Changsha, Hunan, Peoples R China;
10.Cent S Univ, Med Res Ctr, Xiangya Hosp, Changsha, Hunan, Peoples R China;
推荐引用方式
GB/T 7714		 Mao, Chao,Wang, Xiang,Liu, Yating,et al. A G3BP1-Interacting lncRNA Promotes Ferroptosis and Apoptosis in Cancer via Nuclear Sequestration of p53[J]. CANCER RESEARCH,2018,78(13):3484-3496.
APA Mao, Chao.,Wang, Xiang.,Liu, Yating.,Wang, Min.,Bin Yan.,...&Tao, Yongguang.(2018).A G3BP1-Interacting lncRNA Promotes Ferroptosis and Apoptosis in Cancer via Nuclear Sequestration of p53.CANCER RESEARCH,78(13),3484-3496.
MLA Mao, Chao,et al."A G3BP1-Interacting lncRNA Promotes Ferroptosis and Apoptosis in Cancer via Nuclear Sequestration of p53".CANCER RESEARCH 78.13(2018):3484-3496.

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来源：上海药物研究所

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