Lnc-mg is a long non-coding RNA that promotes myogenesis
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ABSTRACT:
PROVIDER: PRJNA360453 | ENA |
REPOSITORIES: ENA
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Project description:Recent studies have indicated important roles for long noncoding RNAs (lncRNAs) as potential essential regulators of myogenesis and adult skeletal muscle regeneration. However, in vivo, the role and mechanism of lncRNAs in myogenic differentiation of adult skeletal muscle stem cells (MuSCs) and myogenesis are still largely unknown. Here, we identified a skeletal muscle specific-enriched lncRNA (myogenesis-associated lncRNA, short for lnc-mg). In vivo, skeletal muscle conditional knockout of lnc-mg resulted in muscle atrophy and the loss of muscular endurance during exercise. Alternatively, skeletal muscle-specific overexpression of lnc-mg promoted muscle hypertrophy in mice. In vitro analyses of primary skeletal muscle cells isolated from mice showed that expression of lnc-mg was increased gradually during myogenic differentiation and overexpressed lnc-mg improved cell differentiation. Mechanistically, lnc-mg promoted myogenesis, by functioning as a competing endogenous RNA (ceRNA) for miR-125b to control protein abundance of Igf2. These findings identify lnc-mg as a novel and important noncoding regulator for muscle cell differentiation and skeletal muscle development. In order to identify functional lncRNAs correlating with myogenesis, microarrays were performed to detect the lncRNAs expression profile in undifferentiated MuSCs (GM, growth media/GM) ) and differentiated MuSCs (DM, differentiation media/DM).
2017-03-01 | GSE93276 | GEO
Project description:Recent studies have indicated important roles for long noncoding RNAs (lncRNAs) as potential essential regulators of myogenesis and adult skeletal muscle regeneration. However, in vivo, the role and mechanism of lncRNAs in myogenic differentiation of adult skeletal muscle stem cells (MuSCs) and myogenesis are still largely unknown. Here, we identified a skeletal muscle specific-enriched lncRNA (myogenesis-associated lncRNA, short for lnc-mg). In vivo, skeletal muscle conditional knockout of lnc-mg resulted in muscle atrophy and the loss of muscular endurance during exercise. Alternatively, skeletal muscle-specific overexpression of lnc-mg promoted muscle hypertrophy in mice. In vitro analyses of primary skeletal muscle cells isolated from mice showed that expression of lnc-mg was increased gradually during myogenic differentiation and overexpressed lnc-mg improved cell differentiation. Mechanistically, lnc-mg promoted myogenesis, by functioning as a competing endogenous RNA (ceRNA) for miR-125b to control protein abundance of Igf2. These findings identify lnc-mg as a novel and important noncoding regulator for muscle cell differentiation and skeletal muscle development. In order to test the hypothesis that lnc-mg may function as a ceRNA leading to the liberation of corresponding miRNA-targeted transcripts, microarrays were performed to detect miRNAs expression in lnc-mg overexpression and lnc-mg knockdown C2C12 cells.
2017-03-01 | GSE93277 | GEO
Project description:Recent studies indicate important roles for long noncoding RNAs (lncRNAs) as essential regulators of myogenesis and adult skeletal muscle regeneration. However, the specific roles of lncRNAs in myogenic differentiation of adult skeletal muscle stem cells and myogenesis are still largely unknown. Here we identify a lncRNA that is specifically enriched in skeletal muscle (myogenesis-associated lncRNA, in short, lnc-mg). In mice, conditional knockout of lnc-mg in skeletal muscle results in muscle atrophy and the loss of muscular endurance during exercise. Alternatively, skeletal muscle-specific overexpression of lnc-mg promotes muscle hypertrophy. In vitro analysis of primary skeletal muscle cells shows that lnc-mg increases gradually during myogenic differentiation and its overexpression improves cell differentiation. Mechanistically, lnc-mg promotes myogenesis, by functioning as a competing endogenous RNA (ceRNA) for microRNA-125b to control protein abundance of insulin-like growth factor 2. These findings identify lnc-mg as a novel noncoding regulator for muscle cell differentiation and skeletal muscle development.
| S-EPMC5353601 | biostudies-literature
Project description:This SuperSeries is composed of the SubSeries listed below.
2017-03-01 | GSE93278 | GEO
Project description:To seek the function of lnc-FANCI-2 in high-risk HPV infected cancer cells, we knocked out lnc-FANCI-2 in CaSki cells (HPV16 positive) using CRISPR/Cas9 system.
2022-06-01 | GSE190904 | GEO
Project description:Effect of a long non-coding RNA, lnc-FANCI-2 on host transcriptome.
| PRJNA788906 | ENA
Project description:Congenital heart defect (CHD) is the most common birth defect worldwide. Copy number variations (CNVs) have been revealed as an important source of pathogenic factor of CHD. 22q11.2 deletion syndrome is the most common microdeletion disorder which has been frequently associated with conotruncal malformations. By now, the dosage sensitive geneTBX1 has been adopted as the major pathogenic gene responsible for 22q11.2 deletion-related heart defects. Here we report the lncRNA lnc-TSSK2-8, which is encompassed in the 22q11.2 region, could activate the canonical Wnt/ -catenin signaling by protecting -catenin from ubiquitination and degradation. Such effects were mediated by two short heat shock proteins HSPA6 and CRYAB, whose expression were regulated by lnc-TSSK2-8 through the ceRNA mechanism. In clinical practice, pathogenesis of CNV were always attributed to haploinsufficiency of protein coding genes. Here we report the 22q11.2 lncRNA lnc-TSSK2-8 significantly activate canonical Wnt/ -catenin signaling, which has major roles in cardiac out flow tract development and should act upstream of TBX1. Our results suggested that lncRNAs should contribute to the etiology of CNV related CHD.
2021-06-02 | GSE165927 | GEO
Project description:Lung Cancer is the leading cause of cancer related deaths worldwide. Unfortunately, radiation resistance is a major problem facing lung cancer patients. Recently, we identified a group of long non-coding RNAs (lncRNAs) known as linc-SPRY3 RNAs, expressed from the Y-chromosome, that play a role in radiation sensitivity by decreasing tumor burden in vitro and in vivo after radiation. In this study, we found that the linc-SPRY3 RNAs are one large lncRNA that we named Radiation Induced Y-chromosome linked long non-coding RNA (lnc-RAINY). Through ATAC-Seq and Immunoprecipitation experiments, we show that lnc-RAINY interacts with DNA in a triple helix to change chromatin opening and gene expression. We also identified that lnc-RAINY regulates CDC6 and CDC25A expression affecting the induction of senescence, inhibition in cell migration, and cell cycle regulation. Furthermore, the administration of nanoparticle encapsulated lnc-RAINY into a lung cancer patient-derived xenograft model dramatically reduces tumor progression demonstrating its therapeutic potential.
2025-04-23 | GSE274485 | GEO
Project description:Lung Cancer is the leading cause of cancer related deaths worldwide. Unfortunately, radiation resistance is a major problem facing lung cancer patients. Recently, we identified a group of long non-coding RNAs (lncRNAs) known as linc-SPRY3 RNAs, expressed from the Y-chromosome, that play a role in radiation sensitivity by decreasing tumor burden in vitro and in vivo after radiation. In this study, we found that the linc-SPRY3 RNAs are one large lncRNA that we named Radiation Induced Y-chromosome linked long non-coding RNA (lnc-RAINY). Through ATAC-Seq and Immunoprecipitation experiments, we show that lnc-RAINY interacts with DNA in a triple helix to change chromatin opening and gene expression. We also identified that lnc-RAINY regulates CDC6 and CDC25A expression affecting the induction of senescence, inhibition in cell migration, and cell cycle regulation. Furthermore, the administration of nanoparticle encapsulated lnc-RAINY into a lung cancer patient-derived xenograft model dramatically reduces tumor progression demonstrating its therapeutic potential.
2025-04-23 | GSE274484 | GEO
Project description:To quantitative analysis of transcriptome changes caused by lnc-OPC knockdown during OPC differentiation from NSC, lentivirus-based short hairpin RNAs were used to knockdown the lnc-OPC expression in a neural stem cell culture . Subsequently, puromycin-selected NSCs were differentiated to OPC in culture for three days.RNA-Seq was performed on the polyadenylated fraction of RNA isolated from cell samples. DEseq was used for differential gene expression analysis caused by lnc-OPC knockdown. GO functional term enrichment analysis of differential gene expression caused by lnc-OPC knockdown, revealed significant enrichment of âoligodendrocyte developmentâ, âoligodendrocyte differentiationâ, âglia cell developmentâ, and âaxon ensheathmentâ terms that are associated with oligodendrogenesis. mRNA profiles of differentiiated NSC samples after lnc-OPC knockdown by RNA-sequencing.
2015-11-04 | E-GEOD-74647 | biostudies-arrayexpress