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CDK7 inhibition by LDC4297 in Mia-Paca2 and Panc89 cells

ABSTRACT: CDK7 inhibition by LDC4297 in Mia-Paca2 and Panc89 cells

PROVIDER: PRJNA797431 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17622415.fastq.gz	Fastqsanger.gz
	SRR17622416.fastq.gz	Fastqsanger.gz
	SRR17622417.fastq.gz	Fastqsanger.gz
	SRR17622418.fastq.gz	Fastqsanger.gz
	SRR17622419.fastq.gz	Fastqsanger.gz

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CDK7 inhibition by LDC4297 in Mia-Paca2 and Panc89 cells

Project description:Inhibition of the dual function cell cycle and transcription kinase CDK7 is known to affect the viability of cancer cells, but the mechanisms underlying cell line-specific growth control remain poorly understood. Here, we employed a previously developed, highly specific small molecule inhibitor that non-covalently blocks ATP binding to CDK7 (LDC4297) to study the mechanisms underlying cell line-specific growth using a panel of genetically heterogeneous human pancre-atic tumor lines as model system. Although LDC4297 diminished both transcription rates and CDK T-loop phosphorylation in a comparable manner, some PDAC lines displayed significantly higher sensitivity than others. We focused our analyses on two well-responsive lines (Mia-Paca2 and Panc89) that, however, showed significant differences in their viability response to extended exposure to limiting LDC4297 concentrations. Biochemical and RNAseq analysis revealed strik-ing differences in gene expression and cell cycle control. Especially the downregulation of a group of cell cycle control genes, among them CDK1/2 and CDC25A/C, correlated well to the observed viability differences in Panc89 versus Mia-Paca2 cells. A parallel downregulation of regulatory pathways supported the hypothesis of a feedforward programmatic effect of CDK7 inhibitors, eventually causing hypersensitivity of PDAC lines.

2022-01-21 | GSE193737 | GEO

MIA-PaCa2 cells transfected with silencer RNA against HuR and YAP1

Project description:Purpose: To determine biological impact between silencing HuR and YAP1, in MIA-PaCa2. Methods: Expression profiling of MIA-PaCa2 cells knocked-down for HuR and YAP1 and control cells transfected with scramble siRNA.

2022-06-07 | GSE167525 | GEO

MIA-PaCa2 cells treated with Pyrvinium Pamoate, Rotenone, Oligomycin or Control

Project description:Purpose: To compared Pyrvinium Pamoate induced transcription changes with known mitochondrial inhibitors. Methods: MIA-PaCa2 cells were treated with Pyrvinium Pamoate at 0.3µM, Oligomycin at 4µM or rotenone at 0.5 µM for 48 hours and then RNA was collected.

2022-06-03 | GSE176305 | GEO

CDK7-dependent Transcriptional Addition in Basal-like Breast Cancer

Project description:Basal-like breast cancer (BBC) is a highly aggressive form of breast cancer that exhibits extremely high levels of genetic complexity and yet a relatively uniform transcriptional program. We postulate that BBC might be highly dependent on uninterrupted transcription of a key set of genes within this gene expression program and might therefore be exceptionally sensitive to inhibitors of transcription. Utilizing a novel kinase inhibitor and CRISPR/Cas9-mediated gene editing, we show here that basal but not luminal breast cancer cells are exceptionally dependent on CDK7, a transcriptional cyclin-dependent kinase. BBC cells are unique in their dependence on this transcriptional CDK and suffer apoptotic cell death upon CDK7 inhibition. An “Achilles cluster” of BBC-specific genes are extremely sensitive to CDK7 inhibition and frequently associated with super-enhancers. We conclude that CDK7 mediates transcriptional addiction to a vital cluster of genes in BBC and CDK7 inhibition may be useful therapy for this challenging cancer. ChIP-Seq for H3K27ac in basal-like breast cancer and luminal-like breast cancer cell lines

2015-01-23 | E-GEOD-65201 | biostudies-arrayexpress

MIA-PaCa2 cells treated with Pyrvinium Pamoate, Rotenone, Oligomycin or Control

Project description:MIA-PaCa2 cells treated with Pyrvinium Pamoate, Rotenone, Oligomycin or Control

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MIA-PaCa2 cells transfected with silencer RNA against HuR and YAP1

Project description:MIA-PaCa2 cells transfected with silencer RNA against HuR and YAP1

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Selective inhibition of CDK7 reveals the influence of CDK7 on psoriatic CD4+ T cells

Project description:Selective inhibition of CDK7 reveals the influence of CDK7 on psoriatic CD4+ T cells

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Targeting of Super-Enhancer-Associated Oncogenic Transcription in MYCN-driven tumor cells by CDK7 inhibition [Gene Expression]

Project description:Global gene expression after CDK7 inhibition by THZ1 Global gene expression after genetic knockdown or overexpression of MYCN

2014-11-21 | E-GEOD-62724 | biostudies-arrayexpress

CDK7 inhibition suppresses RNA polymerase II re-initiation and triggers degradation of elongation and 3'-end processing factors

Project description:CDK7 regulates RNA polymerase II (RNAPII) initiation, elongation, and termination through incompletely-defined mechanisms. Biochemical reconstitution of RNAPII transcription initiation showed that CDK7 inhibition suppressed RNAPII activity by blocking promoter escape and re-initiation and this was Mediator- and TFIID-dependent. These in vitro results were consistent with genomics and transcriptomics experiments in human cells; CDK7 inhibition globally reduced transcription and increased RNAPII promoter-proximal pausing. Moreover, we observed termination defects in CDK7-inhibited cells; unexpectedly, this coincided with rapid, widespread degradation of elongation and 3'-end processing factors. Collectively, these mechanistic insights further define how CDK7 kinase activity regulates RNAPII initiation, termination, and RNA processing.

2024-12-19 | GSE268531 | GEO

CDK7-dependent Transcriptional Addiction in Triple-Negative Breast Cancer (Microarray)

Project description:Triple-negative breast cancer (TNBC) is a highly aggressive form of breast cancer that exhibits extremely high levels of genetic complexity and yet a relatively uniform transcriptional program. We postulate that TNBC might be highly dependent on uninterrupted transcription of a key set of genes within this gene expression program and might therefore be exceptionally sensitive to inhibitors of transcription. Utilizing a novel kinase inhibitor and CRISPR/Cas9-mediated gene editing, we show here that triple-negative but not ER/PR+ breast cancer cells are exceptionally dependent on CDK7, a transcriptional cyclin-dependent kinase. TNBC cells are unique in their dependence on this transcriptional CDK and suffer apoptotic cell death upon CDK7 inhibition. An “Achilles cluster” of TNBC-specific genes are extremely sensitive to CDK7 inhibition and frequently associated with super-enhancers. We conclude that CDK7 mediates transcriptional addiction to a vital cluster of genes in TNBC and CDK7 inhibition may be useful therapy for this challenging cancer. Expression microarrays in H3K27ac in triple-negative breast cancer +/- treatment with covalent CDK7 inhibitor THZ1 treatment

2015-09-24 | E-GEOD-69106 | biostudies-arrayexpress

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