Long noncoding RNA EMS connects c-Myc to cell cycle control and tumorigenesis

被引:65
作者
Wang, Chenfeng [1 ,2 ]
Yang, Yang [1 ,2 ]
Zhang, Guang [1 ,2 ]
Li, Jingxin [1 ,2 ]
Wu, Xianning [3 ]
Ma, Xiaoling [4 ]
Shan, Ge [1 ,2 ]
Mei, Yide [1 ,2 ]
机构
[1] USTC, Sch Life Sci, Hefei Natl Lab Phys Sci Microscale, Div Mol Med,Affiliated Hosp 1, Hefei 230027, Anhui, Peoples R China
[2] USTC, Sch Life Sci, CAS, Key Lab Innate Immun & Chron Dis, Hefei 230027, Anhui, Peoples R China
[3] USTC, Affiliated Hosp 1, Dept Thorac Surg, Hefei 230027, Anhui, Peoples R China
[4] USTC, Affiliated Hosp 1, Dept Lab Med, Hefei 230027, Anhui, Peoples R China
基金
中国国家自然科学基金;
关键词
c-Myc; lncRNA; E2F1; tumorigenesis; TARGET; GENE; E2F; TRANSCRIPTION; EXPRESSION; CANCER; LNCRNA; IDENTIFICATION; MECHANISMS; BIOGENESIS;
D O I
10.1073/pnas.1903432116
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
Deregulated expression of c-Myc is an important molecular hallmark of cancer. The oncogenic function of c-Myc has been largely attributed to its intrinsic nature as a master transcription factor. Here, we report the long noncoding RNA (lncRNA) E2F1 messenger RNA (mRNA) stabilizing factor (EMS) as a direct c-Myc transcriptional target. EMS functions as an oncogenic molecule by promoting G1/S cell cycle progression. Mechanistically, EMS cooperates with the RNA binding protein RALY to stabilize E2F1 mRNA, and thereby increases E2F1 expression. Furthermore, EMS is able to connect c-Myc to cell cycle control and tumorigenesis via modulating E2F1 mRNA stability. Together, these findings reveal a previously unappreciated mechanism through which c-Myc induces E2F1 expression and also implicate EMS as an important player in the regulation of c-Myc function.
引用
收藏
页码:14620 / 14629
页数:10
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