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JMJD6 licenses estrogen receptor alpha-dependent enhancer RNA and coding gene activation by modulating CARM1/MED12 co-activator complex in breast cancer

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE101562 | GEO | 2018/04/16

REPOSITORIES: GEO

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JMJD6 Licenses ER?-Dependent Enhancer and Coding Gene Activation by Modulating the Recruitment of the CARM1/MED12 Co-activator Complex.

Project description: Not available

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JMJD6 licenses estrogen receptor alpha-dependent enhancer RNA and coding gene activation by modulating CARM1/MED12 co-activator complex in breast cancer [ChIP-Seq]

Project description:Enhancers are genomic regulatory elements shown to play key roles in controlling cell type-specific gene expression, regulated by signal-dependent transcription factors and co-factors. Distinct classes of enhancers can specify distinct gene expression profiles and biological outcomes. Recent studies suggested that bidirectional non-coding RNAs (ncRNAs), referred as enhancer RNA (eRNAs), are transcribed on enhancers, which are tightly associated with enhancer activity. However, the protein factors which govern the activation of enhancers remain poorly characterized. Here we reported that a Jumonji C (JmjC) domain-containing protein demethylase, JMJD6, is a determinant for estrogen/estrogen receptor (ER)-induced enhancer activation, coding gene transcription, breast cancer cell growth and tumorigenesis. Mechanistically, JMJD6 was found to be specifically recruited onto ER-bound active enhancers in response to estrogen stimulation, which was required for RNA Pol II recruitment and eRNA production of enhancers, leading to transcriptional activation of cognate estrogen target genes. Furthermore, JMJD6 was found to be physically and functionally associated with MED12 in the mediator complex to regulate estrogen-induced transcriptional activation, with JMJD6 was required for MED12 recruitment onto active enhancers. Specifically, JMJD6 was essential for MED12 to interact with CARM1, an arginine methyltransferase well known to be implicated in estrogen-induced transcriptional activation, which methylated MED12 at its c-terminus at multiple arginine methylation sites and was required for MED12 binding with chromatin. Collectively, our data uncovered a critical regulator of estrogen/estrogen receptor-induced enhancer activation and coding gene transcription, providing a potential drug candidate for developing novel strategies targeting ER-positive breast cancers.

2018-04-16 | GSE101559 | GEO

JMJD6 licenses estrogen receptor alpha-dependent enhancer RNA and coding gene activation by modulating CARM1/MED12 co-activator complex in breast cancer [Gro-Seq]

2018-04-16 | GSE101560 | GEO

JMJD6 licenses estrogen receptor alpha-dependent enhancer RNA and coding gene activation by modulating CARM1/MED12 co-activator complex in breast cancer

Project description:JMJD6 licenses estrogen receptor alpha-dependent enhancer RNA and coding gene activation by modulating CARM1/MED12 co-activator complex in breast cancer

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CARM1 methylates MED12 to regulate its RNA-binding ability.

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Serine 28 phosphorylation of NRIF3 confers its co-activator function for estrogen receptor-alpha transactivation.

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CrkL is a co-activator of estrogen receptor alpha that enhances tumorigenic potential in cancer.

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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

CARM1 mediates the ligand-independent and tamoxifen-resistant activation of the estrogen receptor alpha by cAMP.

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Modulating estrogen receptor-related receptor-alpha activity inhibits cell proliferation.

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