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MAF Amplification licenses Estrogen Receptor α to Drive Breast Cancer Metastasis

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

PROVIDER: PRJNA866475 | ENA |

REPOSITORIES: ENA

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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.

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

| PRJNA971904 | ENA

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 [dataset 2]

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

| PRJNA971507 | ENA

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

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

| PRJNA971172 | ENA

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

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

| PRJNA973608 | ENA

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

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

| PRJNA866479 | ENA

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

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

| PRJNA866480 | ENA

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 [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

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