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Changes in gene expression caused by loss of Med1 in the mouse prostate

ABSTRACT: MED1 is a transcriptional coactivator for gene-specific activators involved in growth and development, we were interested in identifying MED1 target genes potentially involved in prostate development by cDNA microarray. Med1 was conditional knocked out in mice prostate. We performed cDNA microarray with two sets: (1) RNA isolated from three WT ventral prostates and three MT ventral prostates; (2) RNA isolated from three WT lateral prostates and three MT lateral prostates. We used microarrays to detail the global programme of gene expression underlying how Med1 was involved in mice prostate development by regulating targeted genes expression

ORGANISM(S): Mus musculus

PROVIDER: GSE69124 | GEO | 2015/05/22

SECONDARY ACCESSION(S): PRJNA284607

REPOSITORIES: GEO

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Changes in gene expression caused by loss of Med1 in the mouse prostate

Project description:MED1 is a transcriptional coactivator for gene-specific activators involved in growth and development, we were interested in identifying MED1 target genes potentially involved in prostate development by cDNA microarray. Med1 was conditional knocked out in mice prostate. We performed cDNA microarray with two sets: (1) RNA isolated from three WT ventral prostates and three MT ventral prostates; (2) RNA isolated from three WT lateral prostates and three MT lateral prostates. We used microarrays to detail the global programme of gene expression underlying how Med1 was involved in mice prostate development by regulating targeted genes expression 12 mice prostate samples were divided into two groups: (1) three WT ventral prostates and three MT ventral prostates; (2) three WT lateral prostates and three MT lateral prostates.

2015-05-22 | E-GEOD-69124 | biostudies-arrayexpress

Transgenic expression of polyoma virus middle T antigen in the mouse prostate gives rise to carcinoma

Project description:Global gene expression profiles of ventral prostates of wild types and transgenic mice created with MT antigen normal prostate vs prostate cancer induced by MT expression

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Genes up and down regulated in LNCaP cells overexpressing MED1

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Transgenic expression of polyoma virus middle T antigen in the mouse prostate gives rise to carcinoma

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Project description:We performed RNA-seq and ChIP-seq in three prostate cell lines (VCaP, LNCaP and DU145) to ascertain the role of the mediator complex MED1 in AR signaling. Upon androgen stimulation, MED1 undergoes phosphorylation by CDK7 and physically engages with AR at super-enhancer sites, which is essential for AR-mediated transcription. The CDK7 specific inhibitor THZ1 blunts AR-dependent neoplastic growth by preventing the co-recruitment of AR/MED1 in a genome-wide fashion, and reverts the enzalutamide resistance characterized by hyper-phosphorylated MED1. The effect of THZ1 phenocopies that for MED1 and CDK7 knockdown.

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Phosphorylated MED1 Links Transcription Recycling and Cancer Growth

Project description:Mammalian RNA polymerase II (Pol II) initiation, elongation, termination and reinitiation are well studied, but how Pol II dynamically recycles after the transcription cycle remains unclear. By establishing in vitro and in vivo transcription recycling systems, we find that human Mediator 1 (MED1), when phosphorylated at the mammal-specific threonine 1032 by cyclin-dependent kinase 9, dynamically travels with Pol II throughout the transcribed genes to drive Pol II recycling. Mechanistically, MED1 phosphorylation leads to an increase of recycled Pol II via the molecular bridge of MED31, enhancing mRNA output during the transcription recycling process. Importantly, MED1 phosphorylation increases during prostate cancer progression to the lethal phase, and pharmacological inhibition of CDK9 decreases prostate tumor growth through decreasing MED1 phosphorylation and Pol II recycling. Our findings reveal essential mechanisms underlying Pol II recycling and suggest a neglected, yet fundamental Pol II transcription process for therapeutic intervention.

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Med1 overexpression induces cell proliferation

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