Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA125607 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Gene methylation profiling of immortalized human mesenchymal stem cells comparing HPV E6/E7-transfected MSCs cells with human telomerase reverse transcriptase (hTERT)- and HPV E6/E7-transfected MSCs. hTERT may increase gene methylation in MSCs. Goal was to determine the effects of different transfected genes on global gene methylation in MSCs.
2011-08-25 | GSE23936 | GEO
Project description:Gene expression profiling of immortalized human mesenchymal stem cells with hTERT/E6/E7 transfected MSCs. hTERT may change gene expression in MSCs. Goal was to determine the gene expressions of immortalized MSCs.
2010-09-25 | GSE24338 | GEO
Project description:Gene expression profiling of immortalized human mesenchymal stem cells with hTERT/E6/E7 transfected MSCs. hTERT may change gene expression in MSCs. Goal was to determine the gene expressions of immortalized MSCs. One-condition experment, gene expression of 3A6
2010-09-25 | E-GEOD-24338 | biostudies-arrayexpress
Project description:Gene methylation profiling of immortalized human mesenchymal stem cells comparing HPV E6/E7-transfected MSCs cells with human telomerase reverse transcriptase (hTERT)- and HPV E6/E7-transfected MSCs. hTERT may increase gene methylation in MSCs. Goal was to determine the effects of different transfected genes on global gene methylation in MSCs. Two-condition experiment, KP MSCs vs. 3A6 MSCs.
2011-08-24 | E-GEOD-23936 | 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 lentiviral infected prostate cancer cells
| PRJNA260629 | ENA
Project description:Effect of Hotair overexpression in human breast cancer cell lines
| PRJNA294267 | ENA
Project description:Gene expression signatures in GIST-T1 cells transfected with siRNA targeting HOTAIR
| PRJNA147601 | ENA
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 | GSE215289 | 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