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ALDH1A3-mediated gene expression in MDA-MB-231 cells and MDA-MB-468 cells

ABSTRACT: To determine the effect ALDH1A3 expression on global gene expression in MDA-MB-231 cells and MDA-MB-468 cells

ORGANISM(S): Homo sapiens

PROVIDER: GSE49322 | GEO | 2014/02/04

SECONDARY ACCESSION(S): PRJNA213671

REPOSITORIES: GEO

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ALDH1A3-mediated gene expression in MDA-MB-231 cells and MDA-MB-468 cells

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

Expression profiling of MDA-MB-231 and MDA-MB-468 after ALDH1A3 manipulation, all-trans retinoic acid treatment, decitabine treatment

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

DNA methylation profiling of MDA-MB-231 and MDA-MB-468 after ALDH1A3 manipulation, all-trans retinoic acid treatment, decitabine treatment

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RNA-Sequencing of MDA-MB-468 TNBC cells, carboplatin-resistant isogenic MDA-MB-468 cells, and dN90-beta-catenin-overexpressing MDA-MB-468 cells

Project description:In this experiment, we generated isogenic carboplatin-resistant MDA-MB-468 cells displaying a 5x increase in IC50 in respect to the parental cell line. We set out to compare the transcriptome of these cell lines, together with MDA-MB-468 cells overexpressing a constitutively active form of beta-catenin to understand underlying transcriptional changes supporting stable carboplatin-tolerance.

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Expression data from lncRNA AL078604.2 and LINC01269 knockdown in MDA-MB-231, MDA-MB-468 and SKBR3 breast cancer cell lines

Project description:Breast cancer subtype-specific lncRNAs AL078604.2 and LINC01269 were knockdown in breast cancer cell lines LncRNA AL078604.2 was knockdown by an anti-AL076804.2 antisense oligonucleotides (ASOs) in triple-negative breast cancer cell lines MDA-MB-231 and MDA-MB-468 breast cancer cells. LncRNA LINC01269 was knockdown by an anti-LINC01269 ASOs in HER2+ SKBR3 breast cancer cells. To ensure the initial presence of AL078604.2 and LINC01269 in their respective cell lines, qPCR analysis was performed to confirm their expression levels prior to knockdown experiments. The effectiveness of knockdown was confirmed by qPCR analysis, which validated the reduction in AL078604.2 and LNC01269 expression in their corresponding cell lines following ASO treatment.

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