Ontology highlight
ABSTRACT:
PROVIDER: PRJNA260627 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR1572000.fastq.gz | Fastqsanger.gz | |||
| SRR1572001.fastq.gz | Fastqsanger.gz | |||
| SRR1572002.fastq.gz | Fastqsanger.gz | |||
| SRR1572003.fastq.gz | Fastqsanger.gz | |||
| SRR1572004.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 9 |
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Project description:HOTAIR lentiviral infected prostate cancer cells
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Project description:HOTAIR or shHOTAIR lentiviral infected prostate cancer cells [ChIP-Seq]
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Project description:LNCaP prostate cancer cells were infected by lentivirus expressing either ctrl or HOTAIR, and the cells were cultured in hormone-deprived condition (Ethl) or in the presence of androgen (R1881). C4-2B prostate cancer cells were infected by lentivirus expressing either shCtrl or shHOTAIR, and the cells were cultured in hormone-deprived condition (Ethl) or in the presence of androgen (R1881).
2015-10-01 | GSE61268 | GEO
Project description:LNCaP prostate cancer cells were infected by lentivirus expressing either ctrl or HOTAIR. The cells were cultured either in hormone-deprived condition (Ethl) or in the presence of androgen( R1881).
2015-10-01 | GSE61269 | 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.
2010-04-15 | GSE20435 | 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:Short hairpin RNA library-based functional screening identified ribosomal protein L31 that modulates prostate cancer cell growth Vehicle vs. bicalutamide treated LNCaP cells infected with lentiviral shRNA library. Biological replicates: 2 vehicle treatments, 2 bicalutamide treatments.
2015-05-15 | E-GEOD-60382 | biostudies-arrayexpress
Project description:Long noncoding RNA HOTAIR (HOX antisense intergenic RNA) is an important regulator of breast cancer metastasis. Studies showed that HOTAIR reprograms chromatin state through interacting with Polycomb Repressive Complex 2 (PRC2) to promote breast cancer metastasis. However, it is unclear if there exist other HOTAIR-binding factors which participate in promoting breast cancer metastasis. In the current study, we utilized mass spectrometry (ChIRP-MS) to comprehensively identify RNA-binding proteins (RBPs) associated with HOTAIR. We also performed a high-throughput CRISPR screen to investigate HOTAIR-interacting proteins involved in cell metastasis. We found that many m6A-reader proteins were involved in this progress, including YTHDF3, which is a newly identified HOTAIR partner. We further demonstrated that HOTAIR and YTHDF3 co-regulated the expression of several metastasis-associated genes by modifying their chromatin accessibility in breast cancer cells. Altogether, our work detailed the functional interactome of HOTAIR involved in promoting breast cancer cell metastasis, and suggested a mechanism whereby HOTAIR regulates chromatin state in cooperation with the m6A-reader YTHDF3.
2025-10-10 | GSE215284 | GEO
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:The human long noncoding RNA (lncRNA) HOTAIR acts in trans to recruit the Polycomb Repressive Complex 2 (PRC2) to the HOXD gene cluster and promote gene silencing during development. In breast cancers, overexpression of HOTAIR increases metastatic potential via the repression of many additional genes. It has remained unclear what factors determine HOTAIR-dependent PRC2 activity at specific genomic loci, particularly when high levels of HOTAIR result in aberrant gene silencing. To identify additional proteins that contribute to the specific action of HOTAIR, we performed a quantitative proteomic analysis of the HOTAIR interactome. We found that the most specific interaction was between HOTAIR and the heterogeneous nuclear ribonucleoprotein (hnRNP) A2/B1, a member of a family of proteins involved in nascent mRNA processing and RNA matchmaking. Our data suggest that A2/B1 are key contributors to HOTAIR-mediated chromatin regulation in breast cancer cells: A2/B1 knockdown reduces HOTAIR-dependent breast cancer cell invasion and decreases PRC2 activity at the majority of HOTAIR-dependent loci. We found that the B1 isoform, which differs from A2 by 12 additional amino acids, binds with highest specificity to HOTAIR. B1 also binds chromatin and associates preferentially with RNA transcripts of HOTAIR gene targets. We furthermore demonstrate a direct RNA-RNA interaction between HOTAIR and a target transcript that is enhanced by B1 binding. Together, these results suggest a model in which B1 matches HOTAIR with transcripts of target genes on chromatin, leading to repression by PRC2.
2016-05-09 | GSE73702 | GEO