Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA407295 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:We report the H3K27ac status in MDA-MB231 breast cancer cells after knockdown of CDK19 and CDK8.
2019-01-01 | GSE103887 | GEO
Project description:When CDK19 was initially discovered, it was assumed that CDK19 played a redundant role to CDK8 because they share 84% amino acid sequence similarity. However, biological clues such as CDK19s different chromosomal location and its more limited tissue distribution suggested a role distinct from CDK8 To investigate whether CDK19 and CDK8 had distinct biological functions in Triple-Negative breast cancer, we knocked down CDK19 and CDK8 in MDA-MB231 and examined differences in the resulting gene expression.
2020-09-13 | GSE103851 | GEO
Project description:Differential Gene Expression in a Patient-Derived Xenograft from transduction of cells with shRNA targeting CDK19 and CDK8
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Project description:RNA-Seq profiling of triple-negative MDA-MB-231 cell line with know-down of non-canonical WNT signaling receptor Ror1. The MDA-MB231 cells were either transfected with a non-sense control shRNA (shCTL) or with a ROR1 shRNA (shROR1) construct. The objective was to find expression-responsive targets of these perturbations as potential drivers of MDA-MB231 cell invasiveness.
2017-08-17 | GSE96637 | GEO
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
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
Project description:RNA-Seq analysis was carried out to investigate the effects of expression of wild-type CDK8 (CDK8) or CDK19 (CDK19) or their kinase-inactive D173A mutants (CDK8M and CDK19M) in HEK293 cells (WT) and their CDK8/19 double-knockout (dKO) derivatives
2023-06-30 | GSE200753 | GEO
Project description:To study the effect of PIAS1 on transcriptional regulation, we establishedstable PIAS1 shRNA knockdown cells in breast cancer cell line MDA-MB231. By comparing the expression profiles of control vs PIAS1 knockdown cells, we can identify potential PIAS1 target genes involved in breast tumorigenesis. MDA-MB231 Control shRNA and PIAS1 shRNA2 cells were cultured in DMEM plus 10% FBS (DMEM) or SCM for 30 h, and total RNA was used for microarray.
2014-02-06 | E-GEOD-44024 | biostudies-arrayexpress
Project description:When CDK19 was initially discovered, it was assumed that CDK19 played a redundant role to CDK8 because they share 84% amino acid sequence similarity. However, biological clues such as CDK19s different chromosomal location and its more limited tissue distribution suggested a role distinct from CDK8 To investigate whether CDK19 and CDK8 had distinct biological functions in Triple-Negative breast cancer, we knocked down CDK19 and CDK8 in a patient-derived xenograft (PDX-C69) and examined differences in the resulting gene expression.
2018-08-01 | GSE85997 | GEO
Project description:Mfng, a modulator of Notch signaling, is highly expressed in human claudin-low breast cancer (CLBC). To determine Mfng’s roles in CLBC pathogenesis,we knocked down Mfng in a CLBC cell line MDA-MB231, and found that Mfng knockdown altered Notch activation, decreased tumor sphere formation in vitro, and reduced tumor growth in xenograft model. To identify the potential downstream targets of Mfng during CLBC tumorigenesis, we compared the gene expression profiles between xenografts tumor derived from of MDA-MB231 cells carrying Mfng shRNA and the control vector. Mfng, a modulator of Notch signaling, is highly expressed in human claudin-low breast cancer (CLBC). To determine Mfng’s roles in CLBC pathogenesis,we knocked down Mfng in a CLBC cell line MDA-MB231, and found that Mfng knockdown caused alteration in Notch activation, associated with decreased tumor sphere formation in vitro, as well as reduced tumor growth in xenograft model. We intend to compare gene expression profiles between xenografts of MDA-MB231 cells carrying Mfng shRNA and the control vector. This project seeks to identify potential downstream targets of Mfng in CLBC.
2015-05-01 | GSE62481 | GEO