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Expression data from HCT116 colorectal cancer cells.

ABSTRACT: To define the contribution of CDK8 versus CDK19 to gene expression control, we performed a series of microarray assays for cells where each kinase was stably knocked down. Toward this end, we subjected HCT116 cells to three different stress stimuli: 5-fluorouracil (5FU), glucose deprivation, and hypoxia. We found that CDK8, but not CDK19, functions as a widespread coactivator of HIF1A target genes in hypoxia.

ORGANISM(S): Homo sapiens

PROVIDER: GSE38061 | GEO | 2013/03/01

SECONDARY ACCESSION(S): PRJNA167178

REPOSITORIES: GEO

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Expression data from HCT116 colorectal cancer cells.

Project description:To define the contribution of CDK8 versus CDK19 to gene expression control, we performed a series of microarray assays for cells where each kinase was stably knocked down. Toward this end, we subjected HCT116 cells to three different stress stimuli: 5-fluorouracil (5FU), glucose deprivation, and hypoxia. We found that CDK8, but not CDK19, functions as a widespread coactivator of HIF1A target genes in hypoxia. Total RNA from HCT116 cells harvested using an RNeasy kit (Qiagen) was used for gene expression analysis on Affymetrix HuGene 1.0 ST arrays following the manufacturer’s instructions. Differential gene expression was determined with Partek software using one-way ANOVA.

2013-03-01 | E-GEOD-38061 | biostudies-arrayexpress

PolyA RNAseq from HCT116 cells in normoxia and hypoxia

Project description:To determine the effects of depleting TIP60, CDK8, or HIF1A on the transcriptional response to hypoxia, we performed RNAseq analysis of four HCT116 colorectal carcinoma cell lines (shNT, HIF1A-/-, shTIP60 and shCDK8) in normoxic and hypoxic (24hrs, 1% O2) conditions. PolyA RNA for two independent biological replicates was purified from HCT116 cells stably expressing an shRNA against a non-targeting control (shNT), TIP60 (shTIP60) or CDK8 (shCDK8), or genetically deleted HIF1A (HIF1A-/-) subjected to 24hrs 1% O2 (hypoxia) or maintained under ambient oxygen (21%; normoxia) was sequenced on the Ion Torrent platform. Reads were aligned to the human genome and gene-level counts were used for differential expression analysis.

2016-06-02 | E-GEOD-68297 | biostudies-arrayexpress

CDK8 ChIP-seq from HCT116 cells in normoxia and hypoxia

Project description:To test if CDK8 acts directly at HIF1A target genes, we performed ChIP-seq experiments in HCT116 cells under normoxic and hypoxic conditions. ChIP-seq for CDK8 versus Input under normoxia and 24hrs hypoxia (1% O2).

2013-03-01 | E-GEOD-38258 | biostudies-arrayexpress

PolyA RNAseq from HCT116 cells in normoxia and hypoxia

2016-06-02 | GSE68297 | GEO

CDK8 ChIP-seq from HCT116 cells in normoxia and hypoxia

Project description:To test if CDK8 acts directly at HIF1A target genes, we performed ChIP-seq experiments in HCT116 cells under normoxic and hypoxic conditions.

2013-03-01 | GSE38258 | GEO

24hr CA treatment vs. DMSO in HCT116 cells (from 'Identification of CDK8 and CDK19 substrates in human cells using cortistatin A and quantitative phosphoproteomics')

Project description:Cortistatin A (CA) is a highly selective inhibitor of the Mediator kinases CDK8 and CDK19. Using CA, we report here the first large-scale identification of Mediator kinase substrates in human cells (HCT116). Among over 16,000 quantified phosphosites, we identified 78 high-confidence Mediator kinase targets within 64 proteins, including DNA-binding transcription factors and proteins associated with chromatin, DNA repair, and RNA polymerase II. Although RNA-Seq data correlated with Mediator kinase targets, CA effects on gene expression were limited and distinct from CDK8 or CDK19 knockdown. Quantitative proteome analyses, which tracked about 7,000 proteins across six time points (0 â?? 24h), revealed that CA selectively affected pathways implicated in inflammation, growth, and metabolic regulation; contrary to expectations, increased turnover of Mediator kinase targets was not generally observed. Collectively, these data support Mediator kinases as regulators of chromatin and RNA polymerase II activity and suggest cellular roles beyond transcription, including metabolism and DNA repair. HCT116 cells were treated with either 100nM CA or DMSO in biological triplicate for each population (6 samples total). Treatment was for 24h for compound and vehicle.

2016-02-26 | E-GEOD-78506 | biostudies-arrayexpress

PRO-seq from HCT116 cells in normoxia and hypoxia

Project description:PRO-seq analysis was used to examine rapid transcriptional changes in response to short-term hypoxia in WT and HIF1A-/- HCT116 cells

2021-01-29 | GSE145567 | GEO

HIF1A ChIP-seq from HCT116, RKO, A549, and H460 cells in normoxia and hypoxia

Project description:ChIP-seq analysis was used to identify HIF1A binding sites in normoxia and hypoxia in HCT116, RKO, A549, and H460 cells

2021-01-29 | GSE145157 | GEO

12hr 5-FU treatment vs. DMSO in SJSA cells (from 'A kinase independent role for CDK19 in p53 response')

Project description:The human Mediator complex regulates RNA Polymerase II transcription genomewide. A general factor that regulates Mediator function is the four-subunit Mediator kinase module, which contains either CDK8 or CDK19. Whereas CDK8 has been linked to specific signaling cascades and oncogenesis, the cellular roles of its paralog, CDK19, are poorly studied. To define cellular roles for CDK19, we used osteosarcoma cells (SJSA) that naturally lack endogenous CDK8 protein. Although stable CDK19 knockdown was tolerated in SJSA cells, it caused reduced proliferation vs. control shRNA cells. Global gene expression analyses (RNA-Seq) suggested that defects in cholesterol biosynthesis contributed to reduced proliferation in CDK19 knockdown cells (vs. shCTRL). Notably, proliferation defects were rescued with transient expression of wild-type or kinase-dead CDK19. Using RNA-Seq and other assays, we established a general role for CDK19 in the transcriptional response to 5-fluorouracil (5-FU), an inducer of genotoxic and metabolic stress. These experiments also implicated CDK19 in activation of p53 target genes during 5-FU treatment. To further probe a potential role for CDK19 in the p53 response, SJSA cells (shCDK19 vs. shCTRL) were treated with the p53 activator Nutlin-3. Remarkably, CDK19 was required for SJSA cells to return to a proliferative state following Nutlin-3 treatment, and this effect was kinase-independent. These results implicate CDK19 as a regulator of p53 stress responses and suggest a manifestation of CDK19 knockdown—potentially reduced levels of cholesterol metabolites—blocks cellular resistance to Nutlin-3.

2017-05-09 | GSE89807 | GEO

24hr CA treatment vs. DMSO in HCT116 cells (from 'Identification of CDK8 and CDK19 substrates in human cells using cortistatin A and quantitative phosphoproteomics')

Project description:Cortistatin A (CA) is a highly selective inhibitor of the Mediator kinases CDK8 and CDK19. Using CA, we report here the first large-scale identification of Mediator kinase substrates in human cells (HCT116). Among over 16,000 quantified phosphosites, we identified 78 high-confidence Mediator kinase targets within 64 proteins, including DNA-binding transcription factors and proteins associated with chromatin, DNA repair, and RNA polymerase II. Although RNA-Seq data correlated with Mediator kinase targets, CA effects on gene expression were limited and distinct from CDK8 or CDK19 knockdown. Quantitative proteome analyses, which tracked about 7,000 proteins across six time points (0 – 24h), revealed that CA selectively affected pathways implicated in inflammation, growth, and metabolic regulation; contrary to expectations, increased turnover of Mediator kinase targets was not generally observed. Collectively, these data support Mediator kinases as regulators of chromatin and RNA polymerase II activity and suggest cellular roles beyond transcription, including metabolism and DNA repair.

2016-02-26 | GSE78506 | GEO

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