Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA339445 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Normal human mammary epithelial cell (HMLE) and breast cancer MDA-MB-231 cells are engineered to knockdown or enforce expression of variety of LCOR gene products. In addition to wild-type cDNA, functional domain deficient mutants were used to elucidate mechanism of LCOR incorporated transcriptional regulation. The transcriptome profiles were determined and compared.
2017-05-05 | GSE85802 | GEO
Project description:LCOR is a tumor suppressor that induces differentiation of mammary stem cells and cancer stem cells. LCOR orchestrates and sensitizes cells to interferon in ER-negative breast cancer cells. LCOR can act as a co-repressor of activated nuclear receptors and also as a transcription factor by DNA direct binding through its HTH domain. These domains are the most conserved regions of LCOR across vertebrates, suggesting a conserved regulatory function. Here we performed ChiP-seq analysis of LCOR in MDA-MB-231 cells with ectopic expression of the LCOR wild-type, LCOR without the nuclear receptor binding domain (LSKAA) and LCOR with deleted DNA binding domain (HTH). This analysis allows to compare the genome wide distribution of LCOR depending on these specific protein domains
2022-01-04 | GSE163408 | GEO
Project description:GLI1-regulated genes in human mammary epithelial cells and human breast cancer cells
| PRJNA270805 | ENA
Project description:We previously identified a gene signature predicted to regulate the epithelial-mesenchymal transition (EMT) in both epithelial tissue stem cells and breast cancer cells. A phenotypic RNA interference (RNAi) screen identified the genes within this 140-gene signature that promoted the conversion of mesenchymal epithelial cell adhesion molecule-negative (EpCAM-) breast cancer cells to an epithelial EpCAM+/high phenotype. The screen identified 10 of the 140 genes whose individual knockdown was sufficient to promote EpCAM and E-cadherin expression. Among these 10 genes, RNAi silencing of the SWI/SNF chromatin-remodeling factor Smarcd3/Baf60c in EpCAM- breast cancer cells gave the most robust transition from the mesenchymal to epithelial phenotype. Conversely, expression of Smarcd3/Baf60c in immortalized human mammary epithelial cells induced an EMT. The mesenchymal-like phenotype promoted by Smarcd3/Baf60c expression resulted in gene expression changes in human mammary epithelial cells similar to that of claudin-low triple-negative breast cancer cells. These mammary epithelial cells expressing Smarcd3/Baf60c had upregulated Wnt5a expression. Inhibition of Wnt5a by either RNAi knockdown or blocking antibody reversed Smarcd3/Baf60c-induced EMT. Thus, Smarcd3/Baf60c epigenetically regulates EMT by activating WNT signaling pathways. sampleXreference
2013-08-19 | E-GEOD-40145 | biostudies-arrayexpress
Project description:An estrogen-dependent model of breast cancer created by transformation of normal human mammary epithelial cells
| PRJNA98591 | ENA
Project description:LCOR is a corepressor of activated nuclear receptors that inhibits the transcriptional activity of these proteins. Recently, LCOR was described to act also as a transcription activator by DNA direct binding through its HTH domain of genes involved in antigen presentation. This double transcriptional role of LCOR is determined by the expression of nuclear receptor. We overexpressed LCOR and performed RNA-seq in breast cancer cell lines of nuclear receptor positive subtype (MCF7) and nuclear receptor absent (MDA-MB-231). This analysis allows to compare transcriptional regulation of LCOR depending on the presence of nuclear receptors.
2025-11-06 | GSE292767 | GEO
Project description:We previously identified a gene signature predicted to regulate the epithelial-mesenchymal transition (EMT) in both epithelial tissue stem cells and breast cancer cells. A phenotypic RNA interference (RNAi) screen identified the genes within this 140-gene signature that promoted the conversion of mesenchymal epithelial cell adhesion molecule-negative (EpCAM-) breast cancer cells to an epithelial EpCAM+/high phenotype. The screen identified 10 of the 140 genes whose individual knockdown was sufficient to promote EpCAM and E-cadherin expression. Among these 10 genes, RNAi silencing of the SWI/SNF chromatin-remodeling factor Smarcd3/Baf60c in EpCAM- breast cancer cells gave the most robust transition from the mesenchymal to epithelial phenotype. Conversely, expression of Smarcd3/Baf60c in immortalized human mammary epithelial cells induced an EMT. The mesenchymal-like phenotype promoted by Smarcd3/Baf60c expression resulted in gene expression changes in human mammary epithelial cells similar to that of claudin-low triple-negative breast cancer cells. These mammary epithelial cells expressing Smarcd3/Baf60c had upregulated Wnt5a expression. Inhibition of Wnt5a by either RNAi knockdown or blocking antibody reversed Smarcd3/Baf60c-induced EMT. Thus, Smarcd3/Baf60c epigenetically regulates EMT by activating WNT signaling pathways.
2013-08-19 | GSE40145 | GEO
Project description:5AZA-induced Gene Expression in Human Breast Cancer Cell Lines and Benign Primary Mammary Epithelial Cell Cultures
| PRJNA177955 | ENA
Project description:Epithelial cells possess remarkable plasticity, having the ability to become mesenchymal cells through alterations in adhesion and motility (epithelial-to-mesenchymal transition or EMT). Recent studies suggest that EMT endows differentiated epithelial cells with stem cell traits, posing the interesting question of how epithelial plasticity is properly restricted to ensure epithelial differentiation during tissue morphogenesis. Here we identify zinc-finger transcription factor Ovol2 as a key suppressor of EMT of mammary epithelial cells. Epithelia-specific deletion of Ovol2 completely arrests mammary ductal morphogenesis, and depletes epithelial stem/progenitor cell reservoirs. Further, Ovol2-deficient epithelial cells undergo EMT in vivo to become non-epithelial cell types, and that Ovol2 directly represses key EMT inducers such as Zeb1 and regulates stem/progenitor cell responsiveness to TGF-beta. We also provide evidence for a suppressive role of Ovol2 in breast cancer progression. Our findings underscore the critical importance of exquisitely regulating epithelial plasticity to balance stemness with epithelial differentiation in development and cancer. We report ChIPseq data illustrating Ovol2 genome-wide targets in mouse mammary epithelial cells, suggesting that Ovol2 regulates a plethora of genes associated with the EMT process. Immunoprecipitated samples from HC11 mouse mammary epithelial cells with antibodies against Ovol2 and control IgG respectively were used for ChIP-seq experiments.
2014-03-19 | E-GEOD-53925 | biostudies-arrayexpress