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Identification of MAF controlled genes in breast cancer cells

ABSTRACT: To identify relevant genes transcriptionally controlled by MAF in breast cancer, we focused on genes whose expression changed accordingly to MAF transcriptiion factor overexpression in MCF7. We used comparative RNA hybridization (Affymetrix) to this end.

ORGANISM(S): Homo sapiens

PROVIDER: GSE51231 | GEO | 2014/10/01

SECONDARY ACCESSION(S): PRJNA221779

REPOSITORIES: GEO

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Identification of MAF controlled genes in breast cancer cells

Project description:To identify relevant genes transcriptionally controlled by MAF in breast cancer, we focused on genes whose expression changed accordingly to MAF transcriptiion factor overexpression in MCF7. We used comparative RNA hybridization (Affymetrix) to this end. Total RNA from parental and MAFshort or long isoform overexpressing MCF7 grown for 48 hours in regular media (see growth protocol) was isolated from in vitro cultured control and MAF expressing MCF7 parental cells. Total RNA was extracted using the TRIzolM-BM-. Plus RNA Purification Kit (Life Technologies).

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MAF Amplification licenses Estrogen Receptor α to Drive Breast Cancer Metastasis [ATAC-seq]

Project description:We mapped chromatin accessibility on control and MAF-overexpressing MCF7 cells to assess the consequences of estrogen (E2) and metastatic MAF expression on the chromatin landscape. To this end, we cultured MCF7 cells in hormone-deprived (HD) medium for 72 h and estrogen (E2) or vehicle was added for 1h prior to DNA purification. Samples were generated in quadruplicate. We report changes in chromaitn accessibility depending on both MAF expression and E2 stimulation.

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MAF Amplification licenses Estrogen Receptor α to Drive Breast Cancer Metastasis [dataset 1]

Project description:We performed mRNA profiling of control and MAF-overexpressing MCF7 cells to assess the transcriptional consequences of estrogen receptor (ER) activation upon metastatic MAF expression in the presence or absence or ER (using a protac for ER degradation). To this end, we cultured MCF7 cells in hormone-deprived (HD) medium for 72 h. At this point, we treated the cells with vehice or ER-protac for 24h and then estrogen (E2) or vehicle was added for 6h prior to RNA extraction. Samples were generated in triplicate. We report that MAF supports the expression of genes involved in metastatic functions and that E2 treatment and ER expression correlates with E2 early and late gene responses and cell cycle regulation. Additionally, a set of MAF and ER-dependent gene responses was identified. Our results show that MAF expression causes an expansion of ER-mediated transcriptional events in MCF7 cells exposed to E2.

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MAF Amplification licenses Estrogen Receptor α to Drive Breast Cancer Metastasis [ER ChIP-seq]

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Identification of genes associated with bone metastatic breast cancer cells

Project description:We used comparative RNA hybridization (Affymetrix) analysis between Bone metastatic derivatives isolated in vivo and parental cells and focused on changes affecting the expression of potential bone metastasis genes. Total RNA from biological and technical replicates of parental MCF7 and BoM2 bone metastasis derivatives grown for 48 hours in regular media (see growth protocol) was isolated from in vitro cultured control and MAF expressing MCF7 parental cells. Total RNA was extracted using the TRIzolM-BM-. Plus RNA Purification Kit (Life Technologies).

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WT vs c-Maf KO fetal liver macrophage

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