Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA213671 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:To determine the effect ALDH1A3 expression on global gene expression in MDA-MB-231 cells and MDA-MB-468 cells In MDA-MB-231 cells, ALDH1A3 was overexperssed (have low endogenous levels of ALDH1A3) and compared to MSCV empty vector control. In MDA-MB-468 cells that have high endogenous levels of ALDH1A3, ALDH1A3 expresion was reduced with ALDH1A3 shRNA1 and compared to scramble shRNA control.
2014-02-04 | E-GEOD-49322 | biostudies-arrayexpress
Project description:To determine the effect ALDH1A3 expression on global gene expression in MDA-MB-231 cells and MDA-MB-468 cells
2014-02-04 | GSE49322 | GEO
Project description:Retinoids, derivatives of vitamin A, are key physiological molecules with regulatory effects on cell differentiation, proliferation and apoptosis. As a result, they are of interest for cancer therapy. Specifically, models of breast cancer have varied responses to manipulations of the retinoid signaling cascade. This study characterizes the transcriptional response of MDA-MB-231 and MDA-MB-468 breast cancer cells to retinaldehyde dehydrogenase 1A3 (ALDH1A3) and to all-trans retinoic acid (atRA). We demonstrate limited overlap between ALDH1A3-induced gene expression and atRA-induced gene expression in both cell lines, suggesting that the function of ALDH1A3 in breast cancer progression extends beyond its role as a retinaldehyde dehydrogenase. Our data reveals divergent transcriptional responses to atRA, which are largely independent of genomic retinoic acid response elements (RAREs) and consistent with the opposing responses of MDA-MB-231 and MDA-MB-468 to in vivo atRA treatment. We identify transcription factors associated with each gene set. Manipulation of one of the transcription factors (i.e. interferon regulatory factor 1; IRF1) demonstrates that it is the level of atRA-inducible and epigenetically regulated transcription factors that determine expression of target genes (e.g. CTSS, cathepsin S). This study provides a paradigm for complex, combinatorial responses of breast cancer models to atRA treatment, and illustrates the need to characterize RARE-independent responses to atRA in a variety of models.
2017-11-06 | GSE103426 | GEO
Project description:Retinoids, derivatives of vitamin A, are key physiological molecules with regulatory effects on cell differentiation, proliferation and apoptosis. As a result, they are of interest for cancer therapy. Specifically, models of breast cancer have varied responses to manipulations of the retinoid signaling cascade. This study characterizes the transcriptional response of MDA-MB-231 and MDA-MB-468 breast cancer cells to retinaldehyde dehydrogenase 1A3 (ALDH1A3) and to all-trans retinoic acid (atRA). We demonstrate limited overlap between ALDH1A3-induced gene expression and atRA-induced gene expression in both cell lines, suggesting that the function of ALDH1A3 in breast cancer progression extends beyond its role as a retinaldehyde dehydrogenase. Our data reveals divergent transcriptional responses to atRA, which are largely independent of genomic retinoic acid response elements (RAREs) and consistent with the opposing responses of MDA-MB-231 and MDA-MB-468 to in vivo atRA treatment. We identify transcription factors associated with each gene set. Manipulation of one of the transcription factors (i.e. interferon regulatory factor 1; IRF1) demonstrates that it is the level of atRA-inducible and epigenetically regulated transcription factors that determine expression of target genes (e.g. CTSS, cathepsin S). This study provides a paradigm for complex, combinatorial responses of breast cancer models to atRA treatment, and illustrates the need to characterize RARE-independent responses to atRA in a variety of models.
2017-11-06 | GSE103425 | GEO
Project description:Expression profiling of MDA-MB-231 and MDA-MB-468 after ALDH1A3 manipulation, all-trans retinoic acid treatment, decitabine treatment
| PRJNA401792 | ENA
Project description:DNA methylation profiling of MDA-MB-231 and MDA-MB-468 after ALDH1A3 manipulation, all-trans retinoic acid treatment, decitabine treatment
| PRJNA401835 | ENA
Project description:Four cell lines (MCF10A, MCF12A, MDA-MB-231, and MDA-MB-468) were treated with a novel drug candidate.
2020-11-09 | PXD018929 | Pride
Project description:1. Quantitative Proteomics: MDA-MB-231, MDA-MB-468, and MCF12A cells were treated with DMSO (vehicle control) or SU056 (novel small molecule drug candidate). Quantitative proteomics analysis was performed on cell lysates. 2. Cellular Thermal Shift Assay (CETSA): MDA-MB-231 cells were treated with DMSO or SU056 and incubated at different temperatures and protein differences in the resulting soluble and insoluble fractions were determined.3. Cellular Thermal Shift Assay (CETSA): MDA-MB-231 YBOX1 KD cells were treated with DMSO or SU056 and incubated at different temperatures and protein differences in the soluble fractions were determined.
2024-04-04 | PXD042380 | Pride
Project description:To investigate FOXC1 chromatin binding, and the effect of FOXC1 CRISPR knockout in triple negative breast cancer cell lines MDA-MB-231, MDA-MB-468, Hs578t, and Bt-549.
2024-06-14 | GSE213840 | GEO
Project description:To investigate FOXC1 chromatin binding, and the effect of FOXC1 CRISPR knockout in triple negative breast cancer cell lines MDA-MB-231, MDA-MB-468, Hs578t, and Bt-549.
2024-06-14 | GSE213839 | GEO