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LncRNA OIP5-AS1-directed miR-7 degradation promotes MYMX production during human myogenesis

ABSTRACT: LncRNA OIP5-AS1-directed miR-7 degradation promotes MYMX production during human myogenesis

PROVIDER: PRJNA837265 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15312976.fastq.gz	Fastqsanger.gz
	SRR15312977.fastq.gz	Fastqsanger.gz
	SRR15312978.fastq.gz	Fastqsanger.gz
	SRR15312979.fastq.gz	Fastqsanger.gz
	SRR15312980.fastq.gz	Fastqsanger.gz

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LncRNA OIP5-AS1-directed miR-7 degradation promotes MYMX production during human myogenesis

Project description:The goals of this study are to compare differentially expressed RNAs during OIP5-AS1:MIR-7 TSB treated myoblasts and control myoblasts during myogenesis and further investigate functional regulatory network of those RNAs in myogenesis in vitro and in vivo.

2022-06-14 | GSE202752 | GEO

LncRNA OIP5-AS1-directed miR-7 degradation promotes MYMX production during human myogenesis

Project description:LncRNA OIP5-AS1-directed miR-7 degradation promotes MYMX production during human myogenesis

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LncRNA OIP5-AS1/cyrano suppresses GAK expression to control mitosis

Project description:Long noncoding RNAs (lncRNAs) have been found to regulate the expression of mRNAs with which they share partial complementarity. We sought to identify the mechanism through which the lncRNA OIP5-AS1, which is abundant in the cytoplasm, suppressed cell proliferation. Silencing of OIP5-AS1 in human cervical carcinoma cells revealed the appearance of many aberrant (monopolar, multipolar, misaligned) mitotic spindles. By biotin-oligomer affinity pulldown, proteomic, and bioinformatic analyses, we identified a subset of human cell cycle regulatory proteins encoded by mRNAs that were capable of interacting with OIP5-AS1. Further investigation revealed that GAK mRNA, which encodes a cyclin G-associated kinase important for mitotic progression, was a prominent target of OIP5-AS1. The interaction between these two transcripts led to a reduction in GAK mRNA stability and GAK protein abundance, as determined in cells in which OIP5-AS1 levels were increased or decreased. Importantly, the aberrant mitotic cell division seen after silencing OIP5-AS1 was partly rescued if GAK was simultaneously silenced. These findings indicate that the abnormal mitoses seen after silencing OIP5-AS1 was caused by an untimely rise in GAK levels and suggest that OIP5-AS1 suppresses cell proliferation at least in part by reducing GAK levels

2017-09-25 | GSE93551 | GEO

LncRNA OIP5-AS1-directed miR-7 degradation promotes MYMX production during human myogenesis.

Project description:Long noncoding RNAs (lncRNAs) and microRNAs (miRNAs) modulate gene expression programs in physiology and disease. Here, we report a noncoding RNA regulatory network that modulates myoblast fusion into multinucleated myotubes, a process that occurs during muscle development and muscle regeneration after injury. In early stages of human myogenesis, the levels of lncRNA OIP5-AS1 increased, while the levels of miR-7 decreased. Moreover, OIP5-AS1 bound and induced miR-7 decay via target RNA-directed miRNA decay; accordingly, loss of OIP5-AS1 attenuated, while antagonizing miR-7 accelerated, myotube formation. We found that the OIP5-AS1-mediated miR-7 degradation promoted myoblast fusion, as it derepressed the miR-7 target MYMX mRNA, which encodes the fusogenic protein myomixer (MYMX). Remarkably, an oligonucleotide site blocker interfered with the OIP5-AS1-directed miR-7 degradation, allowing miR-7 to accumulate, lowering MYMX production and suppressing myotube formation. These results highlight a mechanism whereby lncRNA OIP5-AS1-mediated miR-7 decay promotes myotube formation by stimulating a myogenic fusion program.

| S-EPMC9262585 | biostudies-literature

LncRNA OIP5-AS1-directed miR-7 degradation promotes MYMX production during human myogenesis

Project description:This SuperSeries is composed of the SubSeries listed below.

2022-06-13 | GSE202793 | GEO

Identification of interacting proteins of lncRNA HIF1α-AS1

Project description:LncRNA Hypoxia-inducible factor 1α-antisense 1 (HIF1α-AS1) is located on the antisense strand of the important Hypoxia-inducible factor 1α (HIF1α) gene, but being transcribed in antisense direction along the HIF1α promoter. Here we used the 3’end biotinylated HIF1a-AS1 RNA and a control RNA for RNA Pulldown and searched for interacting proteins in nuclear extracts of human umbilical vein endothelial cells (HUVEC).

2022-09-23 | PXD023512 | Pride

Identification of protein interaction partners of the lncRNA ADPGK-AS1

Project description:M2-like macrophage upregulated lncRNA ADPGK-AS1 regulates macrophage phenotype and modulates the influence of macrophages on lung tumor apoptosis and migration. Here we identified proteins that interact with ADPGK-AS1 that might give insight into how this regulation this is regulated on molecular level. We were able to identify interaction with mitochondrial ribosomal proteins, leading to regulation of mitochondrial oxidative phosphorylation.

2023-08-13 | PXD030605 | Pride

Circadian lncRNA ADIRF-AS1 binds PBAF and regulates renal clear cell tumorigenesis

Project description:We identified ADIRF-AS1 as a BMAL1-CLOCK regulated circadian lncRNA. Loss of ADIRF-AS1 in U2OS cells altered rhythmicity of clock-controlled genes and expression of genes associated with cell adhesion and the extracellular matrix (ECM) but did not affect neighboring genes in cis. Affinity based enrichment of U2OS ADIRF-AS1-interacting proteins identified all components of the tumor suppressive PBAF (PBRM1/BRG1) complex. Because PBRM1 is a tumor suppressor mutated in 40% of clear cell renal carcinoma (ccRCC) cases, we studied ccRCC 786O cells and also found PBRM1 bound to ADIRF-AS1. Reducing ADIRF-AS1 expression in 786O and A498 ccRCC cells decreased expression of PBAF-suppressed genes, consistent with ADIRF-AS1 acting to antagonize the function of PBAF. Loss of PBRM1, however, rescued PBAF responsive cell cycle genes in ADIRF-AS1 KO 786O ccRCC cells. Importantly, ADIRF-AS1 expression correlates with survival in human ccRCC, particularly in PBRM1 wild-type, but not mutant PBRM1 tumors. In this regard, loss of ADIRF-AS1 did not affect in vitro 786O cell growth, but strikingly eliminated in vivo tumorigenesis, which was partially rescued by concurrent loss of PBRM1. This rescue, however, requires Matrigel, suggesting a PBRM1-independent function of ADIRF-AS1 in regulating the ECM. Collectively, our findings suggest that ADIRF-AS1 functions partly to antagonize the tumor suppressive effect of the PBAF complex and behaves as an unforeseen BMAL1-regulated, oncogenic lncRNA.

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HHIP-AS1 lncRNA promotes tumorigenicity in human SHH-driven brain tumors

Project description:Long non-coding RNAs (lncRNAs) comprise a diverse class of gene expression regulators with emerging roles in many biological processes including cancer. Here we show that the expression of the lncRNA Hedgehog Interacting Protein Antisense 1 (HHIP-AS1) is a hallmark feature of human SHH-driven tumors. Importantly, loss of HHIP-AS1 leads to reduced tumor growth in SHH-driven tumors in vitro and in vivo. Our results demonstrate the power of cross-entity transcriptome-wide comparisons to identify novel epigenetic–regulatory lncRNA circuitries underlying human cancers.

2022-06-01 | PXD016550 | Pride

Knockdown of lncRNA NR2F1-AS1 in gastric cancer cells

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2021-10-07 | GSE183538 | GEO

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