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The lncRNA HOTAIR Modulates DNA-Methylation in Mesenchymal Stem Cells via Triple Helix Formation

ABSTRACT: The lncRNA HOTAIR Modulates DNA-Methylation in Mesenchymal Stem Cells via Triple Helix Formation

PROVIDER: PRJNA285781 | ENA |

REPOSITORIES: ENA

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The lncRNA HOTAIR Modulates DNA-Methylation in Mesenchymal Stem Cells via Triple Helix Formation (expression)

Project description:Long non coding RNAs are implemented in epigenetic changes and regulation of gene expression. HOTAIR is a promising lncRNA concerning epigenetic regulation. We performed HOTAIR overexpression and knockdown experiments in mesenchymal stromal cells derived from bone marrow. After two weeks cells were harvested and RNA and DNA were isolated. Analysis of gene expression was performed with Human Gene 2.0 ST Array (Affymetrix, Santa Clara, USA). Analysis of DNA methylation was performed with Infinium HumanMethylation450 BeadChips (Illumina, San Diego, USA)

2016-11-22 | GSE69492 | GEO

The lncRNA HOTAIR Modulates DNA-Methylation in Mesenchymal Stem Cells via Triple Helix Formation (methylation)

2016-11-22 | GSE69491 | GEO

The lncRNA HOTAIR Modulates DNA-Methylation in Mesenchymal Stem Cells via Triple Helix Formation

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

2016-11-22 | GSE69518 | GEO

The lncRNA HOTAIR impacts on mesenchymal stem cells via triple helix formation.

Project description:There is a growing perception that long non-coding RNAs (lncRNAs) modulate cellular function. In this study, we analyzed the role of the lncRNA HOTAIR in mesenchymal stem cells (MSCs) with particular focus on senescence-associated changes in gene expression and DNA-methylation (DNAm). HOTAIR binding sites were enriched at genomic regions that become hypermethylated with increasing cell culture passage. Overexpression and knockdown of HOTAIR inhibited or stimulated adipogenic differentiation of MSCs, respectively. Modification of HOTAIR expression evoked only very moderate effects on gene expression, particularly of polycomb group target genes. Furthermore, overexpression and knockdown of HOTAIR resulted in DNAm changes at HOTAIR binding sites. Five potential triple helix forming domains were predicted within the HOTAIR sequence based on reverse Hoogsteen hydrogen bonds. Notably, the predicted triple helix target sites for these HOTAIR domains were also enriched in differentially expressed genes and close to DNAm changes upon modulation of HOTAIR Electrophoretic mobility shift assays provided further evidence that HOTAIR domains form RNA-DNA-DNA triplexes with predicted target sites. Our results demonstrate that HOTAIR impacts on differentiation of MSCs and that it is associated with senescence-associated DNAm. Targeting of epigenetic modifiers to relevant loci in the genome may involve triple helix formation with HOTAIR.

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Triple-helix potential of the mouse genome

Project description:Triple-helix potential of the mouse genome

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A single N6-methyladenosine site in lncRNA HOTAIR regulates its function in breast cancer cells

Project description:N6-methyladenosine (m6A) modification of RNA plays important roles in normal and cancer biology, but knowledge of its function on long noncoding RNAs (lncRNAs) remains limited. Here, we investigate whether m6A regulates the function of the human HOTAIR lncRNA, which contributes to multiple pro-tumor phenotypes in triple-negative breast cancer (TNBC) cells. We identify 14 individual m6A sites within HOTAIR, with a single site (A783) consistently methylated. Mutation of A783 impairs cellular proliferation and invasion in HOTAIR-overexpressing TNBC cells. m6A at A783 regulates HOTAIR’s ability to localize to chromatin and induce gene expression changes. A783 mutant HOTAIR reverses wild-type effects beyond baseline, demonstrating a potential antimorphic behavior. HOTAIR interacts with nuclear m6A reader YTHDC1 and YTHDC1-HOTAIR interactions are required for chromatin localization and gene repression. Our work demonstrates how modification of one base in a lncRNA can elicit a distinct gene regulation mechanism and drive disease-associated phenotypic changes.

2021-05-15 | GSE173530 | GEO

RNA-BioID of lncRNA HOTAIR in Flp-In T-REx cells

Project description:Accumulating evidence highlights the role of long non-coding RNAs (lncRNA) in cellular homeostasis, and their dysregulation in disease settings. Most lncRNAs function by interacting with proteins or protein complexes. While several orthogonal methods have been developed to identify these proteins, each method has its inherent strengths and limitations. Here, we combine two RNA-centric methods ChIRP-MS and RNA-BioID to obtain a comprehensive list of proteins that interact with the well-known lncRNA HOTAIR. Overexpression of HOTAIR has been associated with a metastasis-promoting phenotype in various cancers. Although HOTAIR is known to bind with PRC2 and LSD1 protein complexes, an unbiased and comprehensive method to map its interactome has not yet been performed. Both ChIRP-MS and RNA-BioID data sets show an association of HOTAIR with mitoribosomes, suggesting HOTAIR has functions independent of its (post-)transcriptional mode-of-action.

2022-02-15 | PXD029058 | Pride

Next-generation RNA-sequencing data of models of Ewing sarcoma with modulated expression of the lncRNA HOTAIR

Project description:Purpose: Our experimental results demonstrate an essential role for the lncRNA HOTAIR in Ewing sarcoma. We have repressed HOTAIR expression in three Ewing sarcoma cell lines and overexpressed HOTAIR, alone and with EWS-FLI1, in htert-immortalized human mesenchymal stem cells to evaluate its effects on gene expression in this cancer. Methods: RNA-Seq of Ewing sarcoma cell lines with HOTAIR represssed by GapmeR or treated with nonsilencing control, and hTERT-immortalized hMSCs with expression of control GFP, HOTAIR, or HOTAIR and EWS-FLI1, was used for gene expression analysis. Results: Defined gene expression signatures were defined as driven by HOTAIR in each cell line model, with a consensus set of gene identified in the Ewing sarcoma cell lines. Additionally, a set of genes regulated by HOTAIR independently of EWS-FLI1 was identified in the hTERT-hMSC models. Conclusions: HOTAIR expression regulates a set of genes critical to viability, cell adhesion, cell motility, and other markers of EMT and metastasis in Ewing sarcoma, independently of EWS-FLI1.

2018-01-24 | GSE109483 | GEO

LncRNA HOTAIR enhances ER signaling and confers tamoxifen resistance in breast cancer [array]

Project description:HOTAIR is up-regulated in tamoxifen-resistant breast cancer tissues compared to their primary counterparts. Mechanistically, HOTAIR is a direct target of ER-mediated transcriptional repression and is thus restored upon the blockade of ER signaling, either by hormone deprivation or tamoxifen treatment.

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LncRNA HOTAIR enhances ER signaling and confers tamoxifen resistance in breast cancer [ChIP-Seq]

2015-10-01 | GSE71276 | GEO