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RNA-seq analysis evaluating effects of Cdk7 inhibitor THZ1 on responses of mouse hearts to transverse aortic artery constriction (TAC)

ABSTRACT: RNA-seq analysis evaluating effects of Cdk7 inhibitor THZ1 on responses of mouse hearts to TAC

ORGANISM(S): Mus musculus

PROVIDER: GSE151254 | GEO | 2022/04/25

REPOSITORIES: GEO

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RNA-seq analysis evaluating effects of Cdk7 inhibitor THZ1 on responses of mouse hearts to transverse aortic artery constriction (TAC)

Project description:RNA-seq analysis evaluating effects of Cdk7 inhibitor THZ1 on responses of mouse hearts to transverse aortic artery constriction (TAC)

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RNA-seq analysis evaluating effects of Cdk7 inhibitor THZ1 on responses of neonatal rat ventricular myocytes (NRVM) to adrenergic receptor agonist phenylephrine (PE)

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RNA polymerase II (RNAPII) ChIP-seq analysis evaluating effects of Cdk7 inhibitor THZ1 on responses of neonatal rat ventricular myocytes (NRVM) to adrenergic receptor agonist phenylephrine (PE)

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CDK7 inhibitor THZ1 induces the cell apoptosis of B-cell acute lymphocytic leukemia by perturbing cellular metabolism

Project description:Purpose:CDK7 is a potential drug target for the treatment of tumors. THZ1 is the first selective and covalent CDK7 inhibitor, which shows anti-tumor effects in various cancers by inhibiting cell proliferation and inducing apoptosis. However, whether THZ1 has an inhibitory effect on B-ALL cells and the underlying mechanism remains unclear. To address this question, we collected THZ1- and DMSO-treated cells for RNA sequencing Methods:Nalm6 cells were seeded at a density of 1× 10e6 cells/ml and treated with 500nm THZ1or DMSO for 24h. Results:THZ1 perturbed the cellular metabolic pathways of B-ALL cells in vitro.

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RNA sequence analysis of hearts tissue after C57BL/6 mice subjected to transverse aortic constriction (TAC) and dioscin treatment

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THZ1 targeting CDK7 suppresses STAT transcriptional activity and sensitizes T-cell lymphomas to BCL2 inhibitors

Project description:Peripheral T-cell lymphomas (PTCL) are aggressive diseases with poor response to chemotherapy and dismal survival. Identification of effective strategies to target PTCL biology represents an urgent need. Here we report that PTCL are sensitive to transcription-targeting drugs, and, in particular, to THZ1, a covalent inhibitor of cyclin-dependent kinase 7 (CDK7). The STAT-signaling pathway is highly vulnerable to THZ1 even in PTCL cells that carry the activating STAT3 mutation Y640F. In mutant cells, CDK7 inhibition decreases STAT3 chromatin binding and expression of highly transcribed target genes like MYC, PIM1, MCL1, CD30, IL2RA, CDC25A and IL4R. In surviving cells, THZ1 decreases the expression of STAT-regulated anti-apoptotic BH3 family members MCL1 and BCL-XL sensitizing PTCL cells to BH3 mimetic drugs. Accordingly, the combination of THZ1 and the BH3 mimetic obatoclax improves lymphoma growth control in a primary PTCL ex vivo culture and in two STAT3-mutant PTCL xenografts, delineating a potential targeted agent-based therapeutic option for these patients.

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Expression data from mouse heart post transverse aortic constriction (TAC) -surgery 2 weeks

Project description:A number of mediators that have been found to be involved in the pathogenesis of cardiac hypertrophy affecting gene transcription, protein synthesis, metabolism,autophagy, oxidative stress and inﬂammation. These mediators including nuclear transcription factor, microRNAs and long noncoding RNAs. However, the gene expression profiles signaling pathways in the pressure overload-induced cardiac hypertrophy remain unknown. All mice were randomly undertaken sham surgery or TAC for 2 weeks. Hearts were harvested 2 weeks following TAC and performed to further analysis.

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