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

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE210603 | GEO | 2023/09/15

REPOSITORIES: GEO

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MAF Amplification licenses Estrogen Receptor α to Drive Breast Cancer Metastasis [dataset 2]

Project description:We mapped chromatin accessibility on control and MAF-overexpressing MCF7 cells to assess the consequences of estrogen (E2, estrogen cepetor (ER) and metastatic MAF expression on the chromatin landscape. To this end, we cultured MCF7 cells in hormone-deprived (HD) medium for 72 h and a specific ER-protac or vehicle was added for 24h for ER degradation. The day after, estrogen (E2) or vehicle was added for 1h prior to DNA purification. Samples were generated in duplicate. We report changes in chromaitn accessibility depending on both MAF expression and E2 stimulation.

2023-09-15 | GSE232270 | GEO

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

Project description:We performed genome-wide mapping of MAF binding sites in control and MAF-overexpressing MCF7 cells to assess the consequences of estrogen (E2) stimulation on MAF recruitment to chromatin. To this end, we cultured MCF7 cells in hormone-deprived (HD) medium for 72 h and then E2 or vehicle was added for 1h prior to chromatin immunoprecipitation (ChIP). Samples were generated in triplicate. We report that MAF binding is largely independent of E2

2023-09-15 | GSE210605 | GEO

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

Project description:We performed genome-wide mapping of estrogen receptor (ER) binding sites in control and MAF-overexpressing MCF7 cells to assess the consequences of estrogen (E2) stimulation upon metastasic MAF expression. To this end, we cultured MCF7 cells in hormone-deprived (HD) medium for 72 h and then E2 or vehicle was added for 1h prior to chromatin immunoprecipitation (ChIP). Samples were generated in triplicate. We report that E2 induces extensive ER recruitment to chromatin and that ER-binding is gained and expanded upon MAF overexpression.

2023-09-15 | GSE210604 | GEO

MAF Amplification licenses Estrogen Receptor α to Drive Breast Cancer Metastasis.[ChIP-Seq]

Project description:We performed genome-wide mapping of H3k27ac and H3K4me3 sites in control and MAF-overexpressing MCF7 cells to assess the consequences of estrogen (E2) stimulation and MAF overexpression recruitment to chromatin. To this end, we cultured MCF7 cells in hormone-deprived (HD) medium for 72 h and then E2 or vehicle was added for 1h prior to chromatin immunoprecipitation (ChIP). Samples were generated in triplicate.

2023-09-15 | GSE232706 | GEO

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

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. To this end, we cultured MCF7 cells in hormone-deprived (HD) medium for 72 h 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 correlates with E2 early and late gene responses and cell cycle regulation. Additionally, a set of MAF and E2-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. Additionally, we silenced KDM1A expression in MAF-overexpressing MCF7 cells to test whether this histone demethylase mediates the transcriptional consequences of MAF overexpression. Samples with KDM1A knockdown were generated in duplicates. We report that KDM1A partially regulates MAF/E2-dependent gene responses.

2023-09-15 | GSE210607 | GEO

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.

2023-09-15 | GSE232175 | GEO

MAF amplification licenses Estrogen Receptor Alpha to drive breast cancer metastasis

Project description:MAF-amplification increases the risk of breast cancer (BCa) metastasis through poorly understood mechanisms but with important clinical implications. Estrogen receptor-positive (ER+) BCa associated with estrogen (E2) dependency sustains growth of early of breast carcinomas, but ultimately, supports metastasis by unknown mechanisms. Here we integrate proteomics, (epi)genomics and functional assays derived from human and syngeneic BCa mouse models to show that MAF directly interacts with ERalpha, thereby promoting a unique chromatin state that favors the metastatic spread of ER+ BCa cells. Indeed, we identify a set of metastasis-promoting genes that are de novo licenced following EERa2-exposure in a MAF-dependent manner. Among these we found factors influence the establishment of cellular identity and with a known role in metastasis initiation (e.g. SOX9), as well as modulators of the bone stroma, which can ultimately aid in preparing the bone metastatic “soil” (e.g. FGF18, PTHLH and JAG1). Central to the epigenomic remodeling that facilitates the expression of the MAF/E2 gene set is the histone demethylase KDM1A. Indeed, loss of KDM1A activity prevents MAF/E2-mediated BCa metastasis. Collectively, here we disentangle the molecular framework that underlies MAF/E2-mediated metastasis and demonstrate that genetic, epigenetic and hormonal systemic cues are integrated in BCa cells to determine their metastatic success, and with it patient prognosis.

2023-11-13 | PXD035936 | Pride

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).

2014-10-01 | E-GEOD-51231 | biostudies-arrayexpress

Identification of MAF controlled genes in breast cancer cells

2014-10-01 | GSE51231 | GEO

Phosphoproteome of MCF7 breast cancer cells treated with estradiol and BI2536

Project description:Triple SILAC phosphoproteome experiment of hormone deprived MCF7 cells treated with estradiol (E2) in presence or absence of the PLK1 inhibitor BI2536. Conditions were as follows: light (L) population: 1h DMSO, 30min EtOH; medium (M) population: 1h DMSO, 30min E2; heavy (H) population: 1h BI2536, 30min E2. Biological replicates: A and B. Phosphopeptides were enriched from soluble and insoluble fraction using a two step enrichment protocol consiting of strong cation exchange and TiO2 affinity chromatography. The peptides were analyzed on an Orbitrap Velos mass spectrometer linked to an online nanoflow HPLC system via a nanoelectrospray ion source and fragmented via higher-energy C-trap dissociation (HCD). Analysis was carried out using MaxQuant (v. 1.2.2.5) with standard settings including STY phosphporylation as variable modification.

2016-06-24 | PXD000275 | Pride

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