HIF1α-AS1 is a DNA:DNA:RNA triplex-forming lncRNA interacting with the HUSH complex
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE203252 | GEO | 2022/09/23
REPOSITORIES: GEO
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Project description:DNA:DNA:RNA triplexes that are formed through Hoogsteen base-pairing of the RNA in the major groove of the DNA duplex have been observed in vitro, but the extent to which these interactions occur in cells and how they impact cellular functions remains elusive. Using a combination of bioinformatic techniques, RNA/DNA pulldown and biophysical studies, we set out to identify functionally important DNA:DNA:RNA triplex-forming long non-coding RNAs (lncRNA) in human endothelial cells. The lncRNA HIF1α-AS1 was retrieved as a top hit. Endogenous HIF1α-AS1 reduces the expression of numerous genes, including EPH Receptor A2 and Adrenomedullin through DNA:DNA:RNA triplex formation by acting as an adapter for the repressive human silencing hub complex (HUSH). Moreover, the oxygen-sensitive HIF1α-AS1 is down-regulated in pulmonary hypertension and loss-of-function approaches not only result in gene de-repression but also enhance angiogenic capacity. As exemplified here with HIF1α-AS1, DNA:DNA:RNA triplex formation is a functionally important mechanism of trans-acting gene expression control.
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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
Project description:HIF1α-AS1 is a DNA:DNA:RNA triplex-forming lncRNA interacting with the HUSH complex
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Project description:In the current study, on the basis of establishment of PA-induced damage model of HUVECs, the silencing and overexpression (OE) of HIF1A-AS1 were implemented in the HUVECs, and the effects on cell viability, apoptosis, migration and invasion were explored, respectively. Functionally, the results indicated silencing of HIF1A-AS1 promoted the proliferation migration and invasion, and reduced the apoptosis of HUVECs. In contrast, OE of HIF1A-AS1 reduced proliferation transwell and invasion, promoted the apoptosis, suggesting that HIF1A-AS1 play vital roles in regulating HUVECs. Moreover, miRNA sequencing (miRNA-seq) and RNA sequencing (RNA-seq) were carried out, and the results indicated that HIF1A-AS1 globally mediate expression of miRNA and mRNA. The multiple target genes of DEmiRNA were associated with cell proliferation and apoptosis, and overlapped with the DEGs from RNA-seq, suggestion that HIF1A-AS1 might regulate the proliferation and apoptosis of HUVECs by regulating miRNA expression.
2024-06-17 | GSE178401 | GEO
Project description:In the current study, on the basis of establishment of PA-induced damage model of HUVECs, the silencing and overexpression (OE) of HIF1A-AS1 were implemented in the HUVECs, and the effects on cell viability, apoptosis, migration and invasion were explored, respectively. Functionally, the results indicated silencing of HIF1A-AS1 promoted the proliferation migration and invasion, and reduced the apoptosis of HUVECs. In contrast, OE of HIF1A-AS1 reduced proliferation transwell and invasion, promoted the apoptosis, suggesting that HIF1A-AS1 play vital roles in regulating HUVECs. Moreover, miRNA sequencing (miRNA-seq) and RNA sequencing (RNA-seq) were carried out, and the results indicated that HIF1A-AS1 globally mediate expression of miRNA and mRNA. The multiple target genes of DEmiRNA were associated with cell proliferation and apoptosis, and overlapped with the DEGs from RNA-seq, suggestion that HIF1A-AS1 might regulate the proliferation and apoptosis of HUVECs by regulating miRNA expression.
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Project description:Characterisation IER3-AS1 interacting proteins using chromatin oligo-affinity precipitation (ChOP) followed by mass spectrometry. The HeLa cell lysates was incubated with biotinylated antisense oligonucleotides (ASO), targeting an experimental target antisense long noncoding RNA IER3-AS1 or a control RNA LacZ. LacZ and IER3-AS1 interacting proteomes were pulldown using Streptavidin beads. The eluted protein samples from both LacZ control ASOs and IER3-AS1 ASOs subjected to mass-spectrometry analyses to identify IER3-AS1 interacting proteins.
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Project description:In current study, using a lentivirus-based expression system, we observed that overexpressing HIF1A-AS1 successfully promoted apoptosis, significantly altered cell cycle distribution and greatly facilitated migration in VSMCs, further highlighting the robust promoting effects of HIF1A-AS1 to TAA. Moreover, transcriptomics was implemented to uncover its underlying mechanism. A total of 175 differentially expressed genes (DEGs) were identified, with some of them enriched in apoptosis, migration and cell cycle related pathways. Intriguingly, some DEGs were annotated in vascular development or coagulation function pathways. In view of this, we suggested HIF1A-AS1 mediated the progression of TAA by not only regulating the function of VSMC cells, but also altering vascular development or coagulation function. Lastly, RT-qPCR confirmed the veracity and reliability of RNA-sequencing results.
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Project description:Epigenetic dysregulation is a common feature of acute myeloid leukemia (AML). Recently it has become clear that long noncoding RNAs (lncRNAs) can play a key role in epigenetic regulation, and consequently also dysregulation. Currently, our understanding of the requirements and roles of lncRNAs in AML is still limited. Using CRISPRi screening, we identified the lncRNA SGOL1-AS1 as an essential regulator of survival in THP-1 AML cells. We use RNA affinity purification using a biotinylated bait to pull down binding partners of the lncRNA, SGOL1-AS1. The identified proteins show a signficant enrichment for chromatin-modifying proteins involved in gene repression and chromosome organization.
2023-06-12 | PXD034329 | Pride
Project description:Prostate cancer is the most common cancer in men and AR downstream signalings promote prostate cancer cell proliferation. We identified a novel androgen-regulated long non-coding (lnc) RNA, SOCS2-AS1. In order to investigate the SOCS2-AS1 function in prostate cancer cells, we performed gene expression in AR-positive prostate cancer cell lines (LNCaP and LTAD) after siSOCS2-AS1 or siSOCS2 treatment. We also treated cells with vehicle or androgen to analyzed the effects of siSOCS2-AS1 on AR function. Observation of androgen dependent gene expression changes after treatmet with siSOCS2-AS1 with microarray.
2016-08-01 | E-GEOD-82224 | biostudies-arrayexpress
Project description:As the most commonly diagnosed lung cancer, non–small cell lung carcinoma (NSCLC) is regulated by many long noncoding RNAs (lncRNAs). In the present study, we found that SH3PXD2A-AS1 expression in NSCLC tissues was upregulated compared with that in normal lung tissues in The Cancer Genome Atlas (TCGA) database by using the GEPIA website. K-M analysis was performed to explore the effects of this molecule on the survival rate in NSCLC. The results demonstrated that SH3PXD2A-AS1 expression was increased in human NSCLC, and high SH3PXD2A-AS1 expression was correlated with poor overall survival. SH3PXD2A-AS1 promotes lung cancer cell proliferation and accelerates cell cycle progression in vitro. Animal studies validated that knockdown of SH3PXD2A-AS1 inhibits NSCLC cell proliferation in vivo. Mechanically, SH3PXD2A-AS1 interacted with DHX9 to enhance FOXM1 expression, promote tumour cell proliferation and accelerate cell cycle progression. Altogether, SH3PXD2A-AS1 promoted NSCLC growth by interacting with DHX9 to enhance FOXM1 expression. SH3PXD2A-AS1 may serve as a promising predictive biomarker for the diagnosis and prognosis of patients with NSCLC.
2021-08-06 | GSE181195 | GEO