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

2019 ◽  
Vol 116 (29) ◽  
pp. 14620-14629 ◽  
Author(s):  
Chenfeng Wang ◽  
Yang Yang ◽  
Guang Zhang ◽  
Jingxin Li ◽  
Xianning Wu ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Long Noncoding Rna ◽  
Messenger Rna ◽  
Noncoding Rna ◽  
Cell Cycle Progression ◽  
Rna Binding ◽  
Cell Cycle Control ◽  
Intrinsic Nature ◽  
Important Player ◽  
E2f1 Expression

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.

scholarly journals Over-expressed long noncoding RNA HOXA11-AS promotes cell cycle progression and metastasis in gastric cancer

2017 ◽  
Vol 16 (1) ◽  
Author(s):  
Zhili Liu ◽  
Zhenyao Chen ◽  
Ruihua Fan ◽  
Bin Jiang ◽  
Xin Chen ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Cycle ◽  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Cell Cycle Progression ◽  
Cycle Progression

scholarly journals Long Noncoding RNA MALAT1 Controls Cell Cycle Progression by Regulating the Expression of Oncogenic Transcription Factor B-MYB

PLoS Genetics ◽  
2013 ◽  
Vol 9 (3) ◽  
pp. e1003368 ◽  
Author(s):  
Vidisha Tripathi ◽  
Zhen Shen ◽  
Arindam Chakraborty ◽  
Sumanprava Giri ◽  
Susan M. Freier ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Transcription Factor ◽  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Cell Cycle Progression ◽  
Cycle Progression ◽  
Factor B ◽  
Oncogenic Transcription Factor

Long noncoding RNA FOXD2‐AS1 promotes glioma cell cycle progression and proliferation through the FOXD2‐AS1/miR‐31/CDK1 pathway

2019 ◽  
Vol 120 (12) ◽  
pp. 19784-19795 ◽  
Author(s):  
Jin Wang ◽  
Bingqiang Li ◽  
Cunzu Wang ◽  
Yu Luo ◽  
Mengmeng Zhao ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Glioma Cell ◽  
Cell Cycle Progression ◽  
Cycle Progression

scholarly journals The long noncoding RNA Vax2os1 controls the cell cycle progression of photoreceptor progenitors in the mouse retina

RNA ◽  
2011 ◽  
Vol 18 (1) ◽  
pp. 111-123 ◽  
Author(s):  
N. Meola ◽  
M. Pizzo ◽  
G. Alfano ◽  
E. M. Surace ◽  
S. Banfi
Keyword(s):  
Cell Cycle ◽  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Cell Cycle Progression ◽  
Mouse Retina ◽  
Cycle Progression

scholarly journals Long noncoding RNA pncRNA-D reduces cyclin D1 gene expression and arrests cell cycle through RNA m6A modification

2020 ◽  
Vol 295 (17) ◽  
pp. 5626-5639 ◽  
Author(s):  
Ryoma Yoneda ◽  
Naomi Ueda ◽  
Kousuke Uranishi ◽  
Masataka Hirasaki ◽  
Riki Kurokawa
Keyword(s):  
Gene Expression ◽  
Cell Cycle ◽  
Osmotic Stress ◽  
Cyclin D1 ◽  
Hela Cells ◽  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Rna Binding ◽  
Rna Binding Proteins ◽  
Arginine Methylation

pncRNA-D is an irradiation-induced 602-nt long noncoding RNA transcribed from the promoter region of the cyclin D1 (CCND1) gene. CCND1 expression is predicted to be inhibited through an interplay between pncRNA-D and RNA-binding protein TLS/FUS. Because the pncRNA-D–TLS interaction is essential for pncRNA-D–stimulated CCND1 inhibition, here we studied the possible role of RNA modification in this interaction in HeLa cells. We found that osmotic stress induces pncRNA-D by recruiting RNA polymerase II to its promoter. pncRNA-D was highly m6A-methylated in control cells, but osmotic stress reduced the methylation and also arginine methylation of TLS in the nucleus. Knockdown of the m6A modification enzyme methyltransferase-like 3 (METTL3) prolonged the half-life of pncRNA-D, and among the known m6A recognition proteins, YTH domain-containing 1 (YTHDC1) was responsible for binding m6A of pncRNA-D. Knockdown of METTL3 or YTHDC1 also enhanced the interaction of pncRNA-D with TLS, and results from RNA pulldown assays implicated YTHDC1 in the inhibitory effect on the TLS–pncRNA-D interaction. CRISPR/Cas9-mediated deletion of candidate m6A site decreased the m6A level in pncRNA-D and altered its interaction with the RNA-binding proteins. Of note, a reduction in the m6A modification arrested the cell cycle at the G0/G1 phase, and pncRNA-D knockdown partially reversed this arrest. Moreover, pncRNA-D induction in HeLa cells significantly suppressed cell growth. Collectively, these findings suggest that m6A modification of the long noncoding RNA pncRNA-D plays a role in the regulation of CCND1 gene expression and cell cycle progression.

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