Long noncoding RNA EMS connects c-Myc to cell cycle control and tumorigenesis.
basic_science · Level V
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- Record sourced from PubMed, PMID 31262817.
- Also identified by DOI 10.1073/pnas.1903432116 and PMC identifier 6642410.
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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.
Medical subject headings
- Carcinogenesis
- G1 Phase Cell Cycle Checkpoints
- Neoplasms
- Proto-Oncogene Proteins c-myc
- RNA, Long Noncoding