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Effect on gene expression of CDK12/13 inhibition by THZ531 in combination with lapatinib or nilotinib in Hs578T TNBC cells

ABSTRACT: Effect on gene expression of CDK12/13 inhibition by THZ531 in combination with lapatinib or nilotinib in Hs578T TNBC cells

PROVIDER: PRJNA868417 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR21009408.fastq.gz	Fastqsanger.gz
	SRR21009409.fastq.gz	Fastqsanger.gz
	SRR21009410.fastq.gz	Fastqsanger.gz
	SRR21009411.fastq.gz	Fastqsanger.gz
	SRR21009412.fastq.gz	Fastqsanger.gz

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Effect on gene expression of CDK12/13 inhibition by THZ531 in combination with lapatinib or nilotinib in Hs578T TNBC cells

Project description:We performed whole transcriptome expression profiling in Hs578T cells after treatment with THZ531, nilotinib, lapatinib or a combination thereof to study the effect of these combination treatments on the transcriptome.

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Quant-seq analysis to determine the effects of CDK12 and CDK13 inhibition by THZ531 in alternative polyadenylation

Project description:We performed 3' Quant-seq on MV4;11 cells after 6 hours treatment of THZ531 to determine whether CDK12 and CDK13 inhibtion cause alternative polyadenlation

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DRB-PRO-Seq for measuring Pol II transcriptional elongation rate alteration up on CDK12 and CDK13 inhibition by THZ531

Project description:We performed PRO-Seq to measure the Pol II elongation rate by measruing the distance of Pol II travels at viarous time points after relased from DRB induced pausing. We compared DMSO/DRB or THZ531/DRB co-treated sample to assess the effect of CDK12 and CDK13 inhibtion by THZ531 on transcriptional elongation rate.

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Transcriptome wide alternative splicing analysis to determine the effect of CDK12 and CDK13 inhibition by THZ531 in alternative splicing (Total RNA-Seq)

Project description:We performed Total RNA-seq on MV4;11 cells after 6 hours treatment of THZ531 to determine whether CDK12 and CDK13 inhibtion to cause splicing defects.

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Covalent targeting of remote cysteine residues to develop CDK12 and CDK13 inhibitors [Affymetrix]

Project description:Cyclin-dependent kinases 12 and 13 (CDK12 and CDK13) play critical roles in the regulation of gene transcription. However, the absence of CDK12 and CDK13 inhibitors has hindered the ability to investigate the consequences of their inhibition in healthy cells and cancer cells. Here we describe the rational design of a first-in-class CDK12 and CDK13 covalent inhibitor, THZ531. Co-crystallization of THZ531 with CDK12–cyclin K indicates that THZ531 irreversibly targets a cysteine located outside the kinase domain. THZ531 causes a loss of gene expression with concurrent loss of elongating and hyperphosphorylated RNA polymerase II. In particular, THZ531 substantially decreases the expression of DNA damage response genes and key super-enhancer-associated transcription factor genes. Coincident with transcriptional perturbation, THZ531 dramatically induced apoptotic cell death. Small molecules capable of specifically targeting CDK12 and CDK13 may thus help identify cancer subtypes that are particularly dependent on their kinase activities.

2016-08-29 | GSE72022 | GEO

Covalent targeting of remote cysteine residues to develop CDK12 and CDK13 inhibitors [ChIP-Seq]

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Gene expression profiling in melanoma cell lines treated with THZ531 or DMSO

Project description:RNA seq of BRAF-mutated melanoma cell lines (A375 and Colo829) treated with CDK12 inhibitor (THZ531, 500nM) for 6 hours

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Quant-seq analysis of differential polyadenylation site usages in caused by different Pol II mutants with slow elongation rates in Flp-In-293 cells and dual inhibition of CDK12 and CDK13 by THZ531 HEK293T cells

Project description:We used 3' RNA-Seq to determine the effects of slow elongating Pol II on polyadenatltion site usages, also the effects of CDK12 and CDK13 inhibition caused by THZ531 on alternative polyadenylation

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PolyA-sequencing in Jurkat cells upon CDK12 depletion.

Project description:We analyzed the 3' end of polyadenylated transcripts in Jurkat cells treated with either THZ531 (vs. DMSO) or the CDK12 degrader BSJ-4-116 (vs. BSJ-4-116NC).

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Targeting CDK12-mediated transcription regulation in anaplastic thyroid carcinoma [RNA-seq]

Project description:Anaplastic thyroid carcinoma (ATC) is the most aggressive type of thyroid cancer, with no effective treatment available. Identification of new anti-ATC drugs represents an urgent need. In this study, we find that ATC cells are highly sensitive to THZ531, a potent inhibitor of the transcriptional cyclin-dependent kinase (CDK), CDK12. Cell-based assays demonstrate that CDK12 inhibition significantly impedes cell cycle progression, induces apoptotic cell death, and impairs colony formation in ATC cells. THZ531 causes a loss of elongating RNA polymerase II and suppresses gene expression in ATC cells. An integrative analysis of gene expression profiles and super-enhancer landscape, combining with functional assays, leads to the discovery of two new ATC cancer genes, ZC3H4 and NEMP1. Furthermore, CDK12 inhibition enhances the sensitivity of ATC cells to doxorubicin-mediated chemotherapy. Thus, these findings indicate that CDK12 is a potential therapeutic target for ATC treatment and its inhibition may help to overcome the chemoresistance in patients with ATC

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