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Downregulation of MED12 via siRNA in prostate cancer cell lines (3’ tag DGE)

ABSTRACT: Downregulation of MED12 via siRNA in prostate cancer cell lines (3’ tag DGE)

PROVIDER: PRJNA1120050 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29285460.fastq.gz	Fastqsanger.gz
	SRR29285461.fastq.gz	Fastqsanger.gz
	SRR29285462.fastq.gz	Fastqsanger.gz
	SRR29285463.fastq.gz	Fastqsanger.gz
	SRR29285464.fastq.gz	Fastqsanger.gz

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Downregulation of MED12 via siRNA in SPHEROIDS derived from prostate cancer cell lines (3’ tag DGE)

Project description:Downregulation of MED12 via siRNA in SPHEROIDS derived from prostate cancer cell lines (3’ tag DGE)

| PRJNA1120054 | ENA

Downregulation of MED12 via siRNA in prostate cancer cell lines (3’ tag DGE)

Project description:The Mediator complex is a multi-subunit protein that modulates gene expression on a genome-wide scale. MED12 and cyclin-dependent kinase 8 (CDK8) or its paralog CDK19 are components of its kinase module that regulate the proliferation of prostate cancer cells. In this study, we investigated how MED12 and CDK8/19 influence cancer-driven processes in prostate cancer cell lines, focusing on AR activity and enzalutamide resistance.

2024-09-26 | GSE269072 | GEO

Downregulation of MED12 via siRNA in SPHEROIDS derived from prostate cancer cell lines (3’ tag DGE)

2024-09-26 | GSE269073 | GEO

Downregulation of MED12 via siRNA in 22Rv1 prostate cancer cells (full transcriptome)

Project description:Downregulation of MED12 via siRNA in 22Rv1 prostate cancer cells (full transcriptome)

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Downregulation of MED12 via siRNA in 22Rv1 prostate cancer cells (full transcriptome)

2024-09-26 | GSE269070 | GEO

Gene expression data in A172 cell line transfected with MED12 siRNA or its control

Project description:This study identifies the genes differentially expressed upon MED12 knockdown in A172 glioblastoma cell line. Clariom_S_Human Array was used to assess mRNA expression profile in response to MED12 Knockdown in A172 cells.

2022-01-01 | GSE176187 | GEO

Determination of MED12 protein interactome

Project description:Here, the goal of our study was to determine the protein-protein interactome of MED12 in resting and activated human T-cells. We immunoprecipitated endogenous MED12 and evaluated the protein interactome in comparison to an isotype-matched IgG as a control.

2024-12-05 | PXD056255 | Pride

Med12 and p300 chips in HSPCs

Project description:We characterized the genome wide occupancy of Med12 and p300 in mouse HSPCs. We also characterize p300 occupancy upon shRNA against control or Med12. ChIP-seq analysis of Med12 and/or p300 in untreated HSPCs

2016-08-25 | E-GEOD-76053 | biostudies-arrayexpress

Med12 ablation promotes anti-tumor function by enhancing tumor intrinsic immunogenicity in Pancreatic ductal adenocarcinoma [CUT&Tag]

Project description:Pancreatic ductal adenocarcinoma (PDAC) is one of the most lethal cancers with limited treatment options, including checkpoint blockade (ICB) immunotherapy. Epigenetic dysregulation is a defining feature of tumorigenesis and contributes to immune escape. However, little is known about whether and how epigenetic regulators evade immune surveillance in PDAC. Here, we identified Med12, a subunit of RNA polymerase II, as a mediator of immune escape in PDAC with in vivo CRISPR-Cas9 Screening. In murine PDAC models, Med12 loss effectively promoted infiltration and cytotoxicity of CD8+ T cells and NK cells，thereby sensitized to ICB and led to a marked extension of survival. Mechanistically, Med12 loss derepressed endogenous retroelements via impairing H3K9me3 and increasing H3K27Ac modification, triggering cytosolic RNA-sensing and DNA-sensing pathways as well as the type I interferon pathways. Moreover, Med12 depletion induced H3K27Ac gain in the Med12-binding domains, further enhanced the interferon-related genes transcription. Our results demonstrated the role of Med12 in suppressing tumor-intrinsic immunogenicity, thus provided a potential target or marker for immunotherapy of PDAC.

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MED12 mutation activates the tryptophan/kynurenine/AHR pathway to promote growth of uterine leiomyomas

Project description:Uterine leiomyoma (LM) is the most common tumor in women. Estrogen and progesterone, via their receptors ERα and PR, play essential roles in LM growth. Mediator complex subunit 12 (MED12) mutations occur in 70% of all LM and are thought to drive tumor growth in a steroid hormone-dependent manner; however, the mechanisms remain unclear. Here, we performed ChIP-seq (ERα, PR, and MED12) and RNA-seq on LM expressing mutant MED12 (mut-MED12) or wild-type MED12 and matched myometrium. Mut-MED12 altered PR and chromatin interaction landscapes, with significant PR-binding site loss in proximal promoter regions in mut-MED12 LM. Integration of cistrome and transcriptome data identified tryptophan 2,3-dioxygenase (TDO2) as a PR and MED12 target gene, which was aberrantly upregulated in mut-MED12 LM. Kynurenine, the catabolic product of TDO2, was significantly elevated in mut-MED12 LM. Tryptophan or kynurenine treatment of primary LM cells activated the aryl hydrocarbon receptor (AHR) pathway, increased cell proliferation, and inhibited apoptosis; blocking the TDO2-kynurenine-AHR pathway by siRNA knockdown or pharmacologic inhibition abolished these effects. Mut-MED12 LM cells showed higher sensitivity to these treatments. These findings suggest that activation of the TDO2-kynurenine-AHR pathway in mut-MED12 LM induces tumor growth, and may inform the development of targeted treatments and precision medicine in LM.

2023-05-01 | GSE204968 | GEO

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