HOTAIR Modulated Pathways in Early-Stage Breast Cancer Progression
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA758976 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR15671423.fastq.gz | Fastqsanger.gz | |||
| SRR15671423_1.fastq.gz | Fastqsanger.gz | |||
| SRR15671423_2.fastq.gz | Fastqsanger.gz | |||
| SRR15671425.fastq.gz | Fastqsanger.gz | |||
| SRR15671425_1.fastq.gz | Fastqsanger.gz |
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Project description:The long-non-coding HOX transcript antisense intergenic RNA (HOTAIR) was identified as significantly upregulated in breast ductal carcinoma in situ (DCIS). The aim of this study was to characterize the phenotypic effects and signaling pathways modulated by HOTAIR in early-stage breast cancer progression. We determined that HOTAIR induces premalignant phenotypic changes by increasing cell proliferation, migration, invasion and in vivo growth in normal and DCIS breast cell lines. Transcriptomic studies (RNA-seq) identified the main signaling pathways modulated by HOTAIR which include bioprocesses related to cell migration, epithelial to mesenchymal transition, extracellular matrix remodeling and activation of HIF1A, AP1 and FGFR signaling pathways among others. Similar pathways were identified as activated in primary invasive breast carcinomas with HOTAIR over-expression. We conclude that HOTAIR over-expression behaves as a positive regulator of cell growth and migration both in normal and DCIS breast cells involved with early-stage breast cancer progression.
2021-11-01 | GSE183058 | GEO
Project description:The long-non-coding HOX transcript antisense intergenic RNA (HOTAIR) was identified as significantly upregulated in breast ductal carcinoma in situ (DCIS). The aim of this study was to characterize the phenotypic effects and signaling pathways modulated by HOTAIR in early-stage breast cancer progression. We determined that HOTAIR induces premalignant phenotypic changes by increasing cell proliferation, migration, invasion and in vivo growth in normal and DCIS breast cell lines. Transcriptomic studies (RNA-seq) identified the main signaling pathways modulated by HOTAIR which include bioprocesses related to epithelial to mesenchymal transition, cell migration, extracellular matrix remodeling and activation of several signaling pathways (HIF1A, AP1 and FGFR). Similar pathways were identified as activated in primary invasive breast carcinomas with HOTAIR over-expression. We conclude that HOTAIR over-expression behaves as a positive regulator of cell growth and migration both in normal and DCIS breast cells involved with early-stage breast cancer progression.
| S-EPMC8637884 | biostudies-literature
Project description:Previous research has predominantly focused on the regulatory role of lncRNA HOTAIR in gene silencing through its interaction with the Polycomb repressive complex 2 (PRC2). Here, our study uncovers a novel regulatory mechanism of HOTAIR, which facilitates prostate cancer (PCa) progression by sustaining transcription elongation. Using ChIRP-seq, RNA-seq, and ChIP-seq, we successfully mapped the binding sites of HOTAIR across the genome and determined their interplay with the epigenetic landscape. We discovered that the co-localization of HOTAIR with the androgen receptor (AR) can activate gene transcription. In the context of AR binding, we discovered that HOTAIR maintains transcription elongation by facilitating the formation of the CDK9/Pol2S2 complex. We revealed a unique capacity of HOTAIR to promote transcriptional activation on gene promoters/bodies with low H3K27me3 enrichment, a function contrasting to its established PRC2-related transcriptional inhibitory roles in regions with high H3K27me3 signal. Finally, we identified two direct target genes of HOTAIR (MMP14 and TNFAIP2), which contribute to the progression of PCa. Collectively, our research sheds new light on HOTAIR's role in transcriptional regulation, offering potential therapeutic strategies and expand our understanding of HOTAIR's roles in PCa progression.
2024-03-26 | GSE221263 | GEO
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
Project description:This study demonstrated the effects of lncRNA HOTAIR knockdown on the glioma proteomics. An abnormally high expression of the lncRNA HOTAIR has been previously demonstrated in glioma cells. HOTAIR regulates genes by anchoring epigenetic modification proteins and causes abnormalities in multiple signaling pathways. We knocked down HOTAIR in glioma cells by siRNA with SILAC labeling, and then total protein was extracted for proteome mass spectrometry.
2021-12-31 | PXD029919 |
Project description:HOTAIR is a 2.2 kb long noncoding RNA (lncRNA) whose dysregulation has been linked to oncogenesis, defects in pattern formation during early development, and irregularities during the process of epithelial-to-mesenchymal transition (EMT). However, the oncogenic transformation determined by HOTAIR in vivo and its impact on chromatin dynamics are incompletely understood. Here we generate a transgenic mouse model with doxycycline-inducible expression of human HOTAIR in the context of the MMTV-PyMT breast cancer-prone background (iHOT-PyMT mice) to systematically interrogate the cellular mechanisms by which human HOTAIR lncRNA acts to promote breast cancer progression. We isolated breast cancer cells from the primary tumors of iHOT-PyMT mice (named iHOT+ cells) and performed RNA-seq and ATAC-seq of iHOT+ cells treated with 3 conditions: Dox+, Dox- and DoxWD. We showed that HOTAIR overexpression altered both the cellular transcriptome and chromatin accessibility landscape of multiple metastasis-associated genes and promoted epithelial to mesenchymal transition. These alterations are abrogated within several cell cycles after HOTAIR expression is reverted to basal levels, indicating an erasable lncRNA-associated epigenetic memory. These results suggest that a continual role for HOTAIR in programming a metastatic gene regulatory program.
2023-01-10 | GSE201582 | GEO
Project description:MDA-MB-231 Breast Cancer Cells were infected by retroviral expression with either VECTOR or HOTAIR. To test the role of polycomb in HOTAIR mediated gene expression, MDA-MB-231 HOTAIR cells were infected with short hairpin retroviral vectors targeting SUZ12 or EZH2. A genetic modification design type is where an organism(s) has had genetic material removed, rearranged, mutagenized or added, such as knock out. genetic_modification_design
2010-04-15 | E-GEOD-20435 | biostudies-arrayexpress
Project description:Modulated expression of specific tRNA species drives cancer progression
| PRJNA310227 | ENA
Project description:HOTAIR is a 2.2 kb long noncoding RNA (lncRNA) whose dysregulation has been linked to oncogenesis, defects in pattern formation during early development, and irregularities during the process of epithelial-to-mesenchymal transition (EMT). However, the oncogenic transformation determined by HOTAIR in vivo and its impact on chromatin dynamics are incompletely understood. Here we generate a transgenic mouse model with doxycycline-inducible expression of human HOTAIR in the context of the MMTV-PyMT breast cancer-prone background (iHOT-PyMT mice) to systematically interrogate the cellular mechanisms by which human HOTAIR lncRNA acts to promote breast cancer progression. We isolated breast cancer cells from the primary tumors of iHOT-PyMT mice (named iHOT+ cells) and performed RNA-seq and ATAC-seq of iHOT+ cells treated with 3 conditions: Dox+, Dox- and DoxWD. We showed that HOTAIR overexpression altered both the cellular transcriptome and chromatin accessibility landscape of multiple metastasis-associated genes and promoted epithelial to mesenchymal transition. These alterations are abrogated within several cell cycles after HOTAIR expression is reverted to basal levels, indicating an erasable lncRNA-associated epigenetic memory. These results suggest that a continual role for HOTAIR in programming a metastatic gene regulatory program.
2023-01-10 | GSE201581 | GEO
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 | PXD029057 | Pride