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Funding for open access charge: Start-up grant from UIUC. The funders had no role in study design, data collection and analysis. Note = "Funding Information: National Institute of Health American Cancer Society National Science Foundation National Institute on Aging intramural Research Program, NIH Medical University of South Carolina and Hollings Cancer Center (to J.H.Y.) National Institute on Cancer Intramural Research Program, NIH (to A.L.). Our studies have unearthed novel roles played by a MIRHG-encoded lncRNA in regulating RNA binding protein activity, thereby underscoring the importance of determining the function of several hundreds of lnc-miRHGs that are present in human genome.", Further, MIR100HG-depleted cells show reduced interaction between HuR and three of its target mRNAs, indicating that MIR100HG facilitates interaction between HuR and target mRNAs. Notably, MIR100HG interacts with HuR/ELAVL1 as well as with several HuR-target mRNAs. Depletion of MIR100HG-encoded lncRNAs in human cells results in aberrant cell cycle progression without altering the levels of miRNA encoded within MIR100HG. MIR100HG produces spliced and stable lncRNAs that display elevated levels during the G1 phase of the cell cycle. We demonstrate a miRNA-independent role for a nuclear-enriched lnc-miRHG in cell cycle progression. Presently, the cellular function of most lnc-miRHGs is not well understood. A subclass of lncRNAs is synthesized from microRNA (miRNA) host genes (MIRHGs) due to pre-miRNA processing, and are categorized as miRNA-host gene lncRNAs (lnc-miRHGs). Our studies have unearthed novel roles played by a MIRHG-encoded lncRNA in regulating RNA binding protein activity, thereby underscoring the importance of determining the function of several hundreds of lnc-miRHGs that are present in human genome.Ībstract = "Long non-coding RNAs (lncRNAs) regulate vital biological processes, including cell proliferation, differentiation and development. Thus, we demonstrate the role of a S-phase up-regulated lncRNA in cell-cycle progression via modulating the expression of genes controlling cell proliferation.Long non-coding RNAs (lncRNAs) regulate vital biological processes, including cell proliferation, differentiation and development. Finally, elevated SUNO1 levels are associated with poor cancer prognosis and tumorigenicity, implying its pro-survival role. SUNO1 facilitates the cell-cycle-specific transcription of WTIP, a positive regulator of YAP1, by promoting the co-activator, DDX5-mediated stabilization of RNA polymerase II on chromatin. Further, we demonstrate that an S-phase-upregulated lncRNA, SUNO1, facilitates cell-cycle progression by promoting YAP1-mediated gene expression. By performing genome-wide transcriptome analyses in cell-cycle-synchronized cells, we observed cell-cycle phase-specific induction of >2000 lncRNAs. In contrast to the wealth of knowledge of proteins controlling the cell cycle, very little is known about the molecular role of lncRNAs (long noncoding RNAs) in cell-cycle progression. The S-phase-induced lncRNA SUNO1 promotes cell proliferation by controlling YAP1/Hippo signaling pathway.Ĭell cycle is a cellular process that is subject to stringent control.