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Expression data of JMJD6-KO, scramble and wild-type MCF7 cells

ABSTRACT: JMJD6 expression was shown to have different roles in estrogen receptor (ER)-positive and -negative breast cancer cells

ORGANISM(S): Homo sapiens

PROVIDER: GSE216235 | GEO | 2023/01/01

REPOSITORIES: GEO

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Expression data of JMJD6-KO, scramble and wild-type MDA-MB231 cells

Project description:JMJD6 expression was shown to have different roles in estrogen receptor (ER)-positive and -negative breast cancer cells

2023-01-01 | GSE216234 | 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]

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 | GSE101560 | GEO

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

2018-04-16 | GSE101559 | GEO

Expression data of JMJD6-KO, scramble and wild-type MCF7 cells

Project description:Expression data of JMJD6-KO, scramble and wild-type MCF7 cells

| PRJNA892628 | ENA

Bulk and single cell RNA-seq of MCF7 and MCF7 TDP2-KO cells treated with/without estrogen

Project description:To investigate the function of tyrosyl-DNA phosphodiesterase 2 (TDP2) in estrogen receptor (ER) positive breast cancer, we perfomed bulk and single-cell RNA-seq on MCF7 and MCF7 TDP2-KO cells treated with/without estrogen .

2024-04-17 | GSE225423 | GEO

Knock-down and Over-expression of JMJD6 in MCF-7 and/or MDA-MB231

Project description:By survival analysis of breast cancer patients, JMJD6 was found to be significantly associated with poor prognosis. Over-expression and knock-down of JMJD6 in breast cancer cell lines suggested a role in proliferation. In order to study the transcriptional events that occur following JMJD6 expression changes, siRNA-mediated knock-down of JMJD6 was performed in MCF-7 and MDA-MB231 and stable over-expression of JMJD6 was performed in MCF-7. There are 2 different siRNA-mediated knock-downs of JMJD6 with 2 biological replicates in MCF-7 and MDA-MB231; 3 clones of JMJD6 over-expression with 3 biological replicates in MCF-7. The control for the knock-downs is scrambled siRNA-treated MCF-7 and MDA-MB231 and the control for JMJD6 over-expression is empty vector over-expression in MCF-7.

2012-05-09 | E-GEOD-31782 | biostudies-arrayexpress

Expression data of JMJD6-KO, scramble and wild-type MDA-MB231 cells

Project description:Expression data of JMJD6-KO, scramble and wild-type MDA-MB231 cells

| PRJNA892629 | ENA

Expression data of RAW264.7 cells cultured in conditioned medium of SCR or JMJD6-KO PymT-41C cells

Project description:In our study we showed that JMJD6 expression in tumor cells can regulate macrophage differentiation in vitro through ANXA-1 secretion. For this experiment we cultured RAW264.7 cells cultured in conditioned medium of SCR or JMJD6-KO breast cancer PymT-41C cells for 24hrs and we then submitted the RAW264.7 cells for ClariomD assay

2022-01-03 | GSE164399 | GEO

Knock-down and Over-expression of JMJD6 in MCF-7 and/or MDA-MB231

2012-05-10 | GSE31782 | GEO

Transcriptomes of triple-negative breast cancer (TNBC) cells (SUM159) and non-TNBC cells (HCC1569) that overexpressed JMJD6 were compared

Project description:The expression levels of JMJD6 and its correlation with H2A.XY39ph differed in TNBC and non-TNBC cells. In addition, we have previously shown that H2A.XY39ph levels are positively correlated with tumor size, histological grade and advanced TNM stage in breast cancer. To analyze the role of JMJD6 in regulating the characteristics of different subtypes of breast cancer, the transcriptomes of TNBC cells (SUM159) and non-TNBC cells (HCC1569) that overexpressed JMJD6 were compared. We speculate that JMJD6 overexpression cause autophagy pathway activation in TNBC via enhancing ATG genes expression.

2023-10-01 | E-MTAB-6517 | biostudies-arrayexpress

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