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Unknown,Transcriptomics,Genomics,Proteomics

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Expression data from FIT-039 or Flavopiridol compound treated HeLa cells

ABSTRACT: FIT-039 is a novel antiviral compound. Antiviral mechanism of FIT-039 is the inhibition of the viral transcription through suppression of the CTD phosphorylation of RNA polymerase II. We used microarrays to evaluated the effect of FIT-039 on host cellular transcriptome, compared with Flavopiridol which is an existing pan-specific CDK9 inhibitor. HeLa cells were incubated with FIT-039 or flavopiridol at the concentration of IC80 for 24 hr, and cellular RNAs were collected and subjected to microarray analysis. The solvent DMSO was used as a negative control.

ORGANISM(S): Homo sapiens

SUBMITTER: Kei IIDA

PROVIDER: E-GEOD-57429 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Expression data from FIT-039 or Flavopiridol compound treated HeLa cells

Project description:FIT-039 is a novel antiviral compound. Antiviral mechanism of FIT-039 is the inhibition of the viral transcription through suppression of the CTD phosphorylation of RNA polymerase II. We used microarrays to evaluated the effect of FIT-039 on host cellular transcriptome, compared with Flavopiridol which is an existing pan-specific CDK9 inhibitor.

2014-07-08 | GSE57429 | GEO

Flavopiridol profiling on A2780

Project description:The effects of the CDK inhibitor Flavopiridol on the A2780 human adenocarcinoma ovary cell line were analysed by gene expression profiling.

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Flavopiridol profiling on A2780

Project description:The effects of the CDK inhibitor Flavopiridol on the A2780 human adenocarcinoma ovary cell line were analysed by gene expression profiling. A2780 cells were treated with Flavopiridol for 6 hours at a dose equal to 5 times the IC50. Untreated A2780 cells were used as a control. Two replicates per treatment.

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Total RNA Pol2 ChIP-seq in mES cells treated with flavopiridol (Cdk9 inhibitor) after DSIF and NELF knockdown

Project description:Recent studies have found that promoter-proximal pausing occurs at most Pol2-regulated genes. DSIF and NELF function as negative elongation factors and promote Pol2 pausing. P-TEFb, whose enzymatic activity lies in the kinase Cdk9, positively regulates the transition into productive elongation by phosphorylating subunits in DSIF, NELF and Pol2. To gain insights into the interplay between these factors in regulating transcriptional pause release, we tested if knockdown of either pausing factor could bypass P-TEFb function. We find that P-TEFb function is still required for transcriptional elongation after DSIF or NELF knockdown. mES cells were infected with a shRNA hairpin to knockdown Spt5, Spt4, NelfE or control. The resulting cells were then treated with flavopiridol (1uM for 60 minutes). DNA was enriched by chromatin immunoprecipitation (ChIP) and analyzed by Solexa sequencing. A sample of whole cell extract was sequenced and used as the background to determine enrichment. ChIP was performed using an antibody against total RNA Pol2 (Rpb1 N-terminus, Santa Cruz sc-899).

2011-01-19 | E-GEOD-26658 | biostudies-arrayexpress

Flavopiridol in Treating Patients With Refractory Cancer

Project description:RATIONALE: Drugs used in chemotherapy use different ways to stop tumor cells from dividing so they stop growing or die. PURPOSE: Phase I trial to study the effectiveness of flavopiridol in treating patients who have refractory cancer.

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Effects of OGA inhibitor PUGNAc on nascent RNA expression in vivo

Project description:We used 4sU incorporation to detect changes in nascent RNA expression in response to the O-GlcNAc aminidase inhibitor PUGNAc. We found that the distribution of 5' promoter proximal RNAs increased nearly as much as those using the known CDK9 inhibitor flavopiridol. The similar distributions between the known elongation inhibitor flavopiridol and the OGA inhibitor suggested that the PUGNAc blocked RNA pol II elongation in vivo.

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CDK inhibitors and flavopiridol profiling on A2780 and MCF7 cells

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2010-07-14 | E-GEOD-18552 | biostudies-arrayexpress

Homo sapiens

Project description:Expression data from FIT-039 or Flavopiridol compound treated HeLa cells

| PRJNA246447 | ENA

Development of a selective CDK9 degrader from a multi-targeted CDK inhibitor [ChIP-seq]

Project description:Cyclin dependent kinase 9 (CDK9), a key regulator of transcriptional elongation, has long been considered a promising target for cancer therapy, particularly for cancers driven by transcriptional dysregulation. However, despite promising early clinical data in blood cancers using pan-CDK inhibitors that potently inhibit CDK9 such as Dinaciclib and Flavopiridol, no selective CDK9 inhibitors have been clinically approved. Here we show that a multi-targeted CDK inhibitor can be used to develop a selective CDK9 degrader exemplified by THAL-SNS-032, a hetero-bifunctional molecule composed of SNS-032, a CDK2,7,9 inhibitor conjugated to thalidomide, a small molecule binder of Cereblon. We demonstrate that THAL-SNS-032 can recruit the E3 ubiquitin ligase Cereblon to CDK9 and induce its proteasome-mediated degradation. Treatment of cells with low nanomolar concentrations of THAL-SNS-032 resulted in rapid and efficient CDK9 degradation but did not affect levels of other SNS-032 targets, including CDK2 and CDK7. Consistent with this selective degradation phenotype, transcriptional profiling of THAL-SNS-032 indicated that its transcriptional effects were more similar to that of a selective CDK9 inhibitor, NVP2, than that of the nonselective SNS-032 parent compound. Moreover, THAL-SNS-032, in contrast to traditional CDK9 inhibitors, retained potent pro-apoptotic activity even after compound removal from cells. This suggests that degradation of CDK9 leads to prolonged cytotoxic effects as compared to CDK9 inhibition. Thus, our findings suggest that thalidomide conjugation may be a promising strategy for converting multi-targeting inhibitors into selective degraders, and that the pharmacological effects of kinase degradation can be distinct from kinase inhibition.

2017-09-01 | GSE89384 | GEO

Development of a selective CDK9 degrader from a multi-targeted CDK inhibitor [RNA-seq]

2017-09-01 | GSE89385 | GEO