长非编码 RNA EMS 将 c-Myc 与细胞周期控制和肿瘤发生联系起来。
Long noncoding RNA EMS connects c-Myc to cell cycle control and tumorigenesis.
机构信息
Division of Molecular Medicine, Hefei National Laboratory for Physical Sciences at Microscale, First Affiliated Hospital of University of Science and Technology of China, School of Life Sciences, University of Science and Technology of China (USTC), 230027 Hefei, Anhui, China.
Chinese Academy of Sciences (CAS) Key Laboratory of Innate Immunity and Chronic Disease, School of Life Sciences, USTC, 230027 Hefei, Anhui, China.
出版信息
Proc Natl Acad Sci U S A. 2019 Jul 16;116(29):14620-14629. doi: 10.1073/pnas.1903432116. Epub 2019 Jul 1.
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.
c-Myc 的失调表达是癌症的一个重要分子标志。c-Myc 的致癌功能在很大程度上归因于其作为主转录因子的固有性质。在这里，我们报告长非编码 RNA (lncRNA) E2F1 信使 RNA(mRNA)稳定因子 (EMS) 是 c-Myc 的直接转录靶标。EMS 通过促进 G1/S 细胞周期进程发挥致癌分子的作用。从机制上讲，EMS 与 RNA 结合蛋白 RALY 合作稳定 E2F1 mRNA，从而增加 E2F1 的表达。此外，EMS 能够通过调节 E2F1 mRNA 的稳定性将 c-Myc 与细胞周期控制和肿瘤发生联系起来。总之，这些发现揭示了 c-Myc 诱导 E2F1 表达的一个以前未被认识的机制，并暗示 EMS 是调节 c-Myc 功能的一个重要参与者。
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