Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA316330 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:We report high-throughput profiling of TRIM25 binding sites in triple negative breast cancer cells.
2017-04-01 | GSE79588 | GEO
Project description:We report high-throughput profiling of TRIM25 bound mRNA in triple negative breast cancer cells.
2017-04-01 | GSE79587 | GEO
Project description:Identification of mRNA bound by TRIM25 binding in triple negative breast cancer
| PRJNA316331 | ENA
Project description:We have utilized ChIPseq to identify the ER-beta cistrome in ER-beta expressing MDA-MB-231 triple negative breast cancer cells. ER-beta has been identified as a tumor suppressor in breast cancer and recent reports have demonstrated that ER-beta protein is detectable at moderate to high levels in approximately 30% of triple negative breast tumors. Increased expression of ER-beta in triple negative breast cancer has also been reported to be associated with improved recurrence-free survival. Treatment of ER-beta expressing triple negative breast cancer cells with estrogen, or the ER-beta selective agonist, LY500307, results in decreased cell proliferation, invasion and migration. To begin to identify the molecular mechanisms by which ER-beta elicits tumor suppressive effects in triple negative breast cancer, we performed ChIPseq studies and identified the genome-wide binding sites for ER-beta following exposure to 1nM estrogen or 10nM LY500307 for 3 hours. Over 28,000 and 10,000 unique ER-beta binding sites were identifed in response to these two ligands respectively. The top transcription factor motifs identified under both treatment conditions were estrogen response elements and AP1 response elements. The majority of ER-beta binding sites were found at enhancer regions located within introns or intergenic chromatin regions followed by gene promoters.
2018-08-23 | GSE108979 | GEO
Project description:We report the application of ChIP-seq, which combines chromatin immunoprecipitation (ChIP) with massively parallel DNA sequencing, to map genome-wide XBP1 binding sites in different breast cancer cell lines. We showed that HIF1M-NM-1 motif was enriched in XBP1 binding sites in triple negative breast cancer (TNBC) cell lines, but not enriched in ER positive breast cancer cell line. We also demonstrated that different breast cancer cell lines of the same sub-type had similar XBP1 binding sites, whereas different breast cancer sub-types had majorly different XBP1 binding sites. Finally, a model was applied to integrate XBP1 ChIP-seq data with expression data to predict XBP1's direct targets in TNBC cell line; the predicted direct targets were shown to be predictive of patient survival, and the prediction power was specific to TNBC patients. The above evidence indicates that XBP1 performs important functions in TNBC by interacting with HIF1M-NM-1, and such regulation mechanism is specific to TNBC, which is later proved by follow-up experiments.This study represents the first detailed anaysis of XBP1 binding sites in different breast cancer cell lines. Examination of XBP1 binding sites in 2 cell types (3 cell lines).
2013-09-26 | E-GEOD-49952 | biostudies-arrayexpress
Project description:This experiment is performed to reveal the novel binding sites of Snai1 transcription factor globally in triple negative breast cancer cell line Hs578T. We also reveal the effect of TGF cytokine on the binding sites of Snai1.
2018-04-25 | E-MTAB-5242 | biostudies-arrayexpress
Project description:This experiment is performed to reveal the novel binding sites of ZEB1 transcription factor globally in triple negative breast cancer cell line Hs578T. We also reveal the effect of TGF cytokine on the binding sites of ZEB1.
2018-04-25 | E-MTAB-5241 | biostudies-arrayexpress
Project description:Using CHIRP-MS method to detect LINC00461 binding protein in MDA-MB-231 cell line of triple negative breast cancer
2023-04-04 | PXD041363 | iProX
Project description:We report the application of ChIP-seq, which combines chromatin immunoprecipitation (ChIP) with massively parallel DNA sequencing, to map genome-wide XBP1 binding sites in different breast cancer cell lines. We showed that HIF1α motif was enriched in XBP1 binding sites in triple negative breast cancer (TNBC) cell lines, but not enriched in ER positive breast cancer cell line. We also demonstrated that different breast cancer cell lines of the same sub-type had similar XBP1 binding sites, whereas different breast cancer sub-types had majorly different XBP1 binding sites. Finally, a model was applied to integrate XBP1 ChIP-seq data with expression data to predict XBP1's direct targets in TNBC cell line; the predicted direct targets were shown to be predictive of patient survival, and the prediction power was specific to TNBC patients. The above evidence indicates that XBP1 performs important functions in TNBC by interacting with HIF1α, and such regulation mechanism is specific to TNBC, which is later proved by follow-up experiments.This study represents the first detailed anaysis of XBP1 binding sites in different breast cancer cell lines.
2013-09-26 | GSE49952 | GEO