Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

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

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

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

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

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

| PRJNA866478 | ENA

MAF Amplification licenses Estrogen Receptor α to Drive Breast Cancer Metastasis

Project description:MAF Amplification licenses Estrogen Receptor α to Drive Breast Cancer Metastasis

| PRJNA866475 | ENA

MAF Amplification licenses Estrogen Receptor α to Drive Breast Cancer Metastasis.

Project description:MAF Amplification licenses Estrogen Receptor α to Drive Breast Cancer Metastasis.

| PRJNA971904 | ENA