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AKT/ERK-mediated activation of CDK7-MED1-AR axis drives resistance to pan BET bromodomain inhibitor ZEN-3694 in advanced prostate cancer [RNA-Seq]

ABSTRACT: AKT/ERK-mediated activation of CDK7-MED1-AR axis drives resistance to pan BET bromodomain inhibitor ZEN-3694 in advanced prostate cancer [RNA-Seq]

PROVIDER: PRJNA810969 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18163230_1.fastq.gz	Fastqsanger.gz
	SRR18163230_2.fastq.gz	Fastqsanger.gz
	SRR18163231_1.fastq.gz	Fastqsanger.gz
	SRR18163231_2.fastq.gz	Fastqsanger.gz
	SRR18163232_1.fastq.gz	Fastqsanger.gz

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AKT/ERK-mediated activation of CDK7-MED1-AR axis drives resistance to pan BET bromodomain inhibitor ZEN-3694 in advanced prostate cancer

Project description:AKT/ERK-mediated activation of CDK7-MED1-AR axis drives resistance to pan BET bromodomain inhibitor ZEN-3694 in advanced prostate cancer

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AKT/ERK-mediated activation of CDK7-MED1-AR axis drives resistance to pan BET bromodomain inhibitor ZEN-3694 in advanced prostate cancer [Exome-Seq]

Project description:AKT/ERK-mediated activation of CDK7-MED1-AR axis drives resistance to pan BET bromodomain inhibitor ZEN-3694 in advanced prostate cancer [Exome-Seq]

| PRJNA812027 | ENA

AKT/ERK-mediated activation of CDK7-MED1-AR axis drives resistance to pan BET bromodomain inhibitor ZEN-3694 in advanced prostate cancer [RNA-Seq]

Project description:Prostate cancer cells were cultured in the presence of the drug Zenith-3694 for a period of 16-20 weeks to develop drug-resistant cells and subjected to RNA sequencing.

2022-03-05 | GSE197557 | GEO

AKT/ERK-mediated activation of CDK7-MED1-AR axis drives resistance to pan BET bromodomain inhibitor ZEN-3694 in advanced prostate cancer [Exome-Seq]

Project description:Prostate cancer cells were cultured in the presence of the drug Zenith-3694 for a period of 16-20 weeks to develop drug-resistant cells and subjected to Exome sequencing.

2022-03-05 | GSE197772 | GEO

CDK7 inhibition suppresses Castration-Resistant Prostate Cancer through MED1 inactivation

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.

2019-08-20 | GSE125245 | GEO

CDK7 inhibition suppresses Castration-Resistant Prostate Cancer through MED1 inactivation

Project description:CDK7 inhibition suppresses Castration-Resistant Prostate Cancer through MED1 inactivation

| PRJNA515688 | ENA

AKT/ERK-mediated activation of CDK7-MED1-AR axis drives resistance to pan BET bromodomain inhibitor ZEN-3694 in advanced prostate cancer

Project description:This SuperSeries is composed of the SubSeries listed below.

2022-03-05 | GSE197773 | GEO

Neurospora crassa strain:3694

Project description:Neurospora crassa 3694 Resequencing

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Primary murine embryonic fibroblasts (MEFs): Cdk7 wild type versus Cdk7 KO

Project description:Transcriptional profiling of primary Cdk7lox/lox MEFs comparing Adeno-Cre vs Adeno-GFP infected controls. Samples were obtained 7 days after the Adeno-Cre mediated elimination of Cdk7. Goal was to determine the effects of Cdk7 elimination on RNA polII-mediated transcription. Two-condition experiment, Adeno-Cre vs. Adeno-GFP infected Cdk7lox/lox MEFs. Biological replicates: 10 independent primary MEF preparations.

2012-04-17 | E-GEOD-36050 | biostudies-arrayexpress

Targeting transcriptional dependencies in cancer using a covalent CDK7 inhibitor (expression)

Project description:Cyclin-dependent kinase 7 (CDK7) plays a critical role in the general regulation of RNA polymerase II-mediated transcription. However, the absence of selective CDK7 inhibitors has hindered the ability to investigate the consequences of acute and prolonged inhibition of CDK7 under normal and pathological conditions. Here we present the discovery and characterization of the first covalent CDK7 inhibitor, CDK7-IN-1, that has the unprecedented ability to target a unique cysteine residue located outside of the canonical kinase domain, providing an unanticipated means of achieving selectivity for CDK7 amongst the 20 known CDKs. Cancer cell line profiling indicates that a subset of cancer cell lines, including T-cell acute lymphoblastic leukemia (T-ALL), exhibit 100-fold greater sensitivity to CDK7-IN-1 over other tumor and normal cell lines. Genome-wide expression analysis in Jurkat T-ALL indicates that CDK7-IN-1 disproportionally affects RUNX1 as well as other components of the TAL1 transcriptional network and its targets, downregulating key regulators of transcription and apoptosis critical for the T-ALL state. These oncogenes are encoded by short-lived mRNA transcripts, are associated with super-enhancers, and exhibit a strong dependency on continuous transcription for sustained expression. Therefore, pharmacological modulation of CDK7 kinase activity may define a method for the identification and treatment of tumor types exhibiting extreme dependencies on transcription for maintenance of the oncogenic state. Jurkat, MM1S, Loucy, and HeLa (WT and Dox-inducible CDK7 mutant) cells were treated with various drugs including a covalent inhibitor of CDK7 (CDK7-IN-1), a reversible inhibitor of CDK7 (CDK7-IN-1), Flavopiridol, Actinomycin D, and DMSO controls. Replicates are annotated.

2014-06-22 | E-GEOD-50624 | biostudies-arrayexpress

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