| Literature DB >> 31262817 |
Chenfeng Wang1,2, Yang Yang1,2, Guang Zhang1,2, Jingxin Li1,2, Xianning Wu3, Xiaoling Ma4, Ge Shan1,2, Yide Mei5,2.
Abstract
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.Entities:
Keywords: E2F1; c-Myc; lncRNA; tumorigenesis
Year: 2019 PMID: 31262817 PMCID: PMC6642410 DOI: 10.1073/pnas.1903432116
Source DB: PubMed Journal: Proc Natl Acad Sci U S A ISSN: 0027-8424 Impact factor: 11.205