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RNAseq of U87 treated with bulk control/0.5mM 8-cpt-cAMP/1nM MS275 or a combination

ABSTRACT: Transcriptomics revealed that the combination of 8-cpt-cAMP and MS275 could maximize the glioma differentation compared to control or use either drug alone

ORGANISM(S): Homo sapiens

PROVIDER: GSE158015 | GEO | 2023/03/15

REPOSITORIES: GEO

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RNAseq of U87/over-expressed DPF3 U87 treated with bulk control/0.5mM 8-cpt-cAMP combination with 1nM MS275 for 48hrs

Project description:Transcriptomics revealed that the combination of 8-cpt-cAMP and MS275 could maximize the glioma differentation compared to control or use either drug alone

2020-09-17 | GSE158065 | GEO

RNAseq and the histone acetylated chromosome immunoprecipitation of U87 or GBM stem cells(GSC) treated with bulk control/0.5mM 8-cpt-cAMP/1nM MS275 or a combination

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RNAseq of U87/over-expressed DPF3 U87 treated with bulk control/0.5mM 8-cpt-cAMP combination with 1nM MS275 for 48hrs

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ChIP-seq of H3K9ac and H3K14ac in U87 glioma cells treated with differentiation agents(0.5mM 8-cpt-cAMP combined with 1nM MS275) for 48h

Project description:ChIP-seq of H3K9ac and H3K14ac in U87 glioma cells treated with differentiation agents(0.5mM 8-cpt-cAMP combined with 1nM MS275) for 48h

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ChIP-seq of H3K9ac and H3K14ac in U87 glioma cells treated with differentiation agents(0.5mM 8-cpt-cAMP combined with 1nM MS275) for 48h

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2020-09-22 | GSE158272 | GEO

Timecourse of Gene Expression responses to cAMP in S49 Cells

Project description:Abstract Although a substantial number of hormones and drugs increase cellular cAMP levels, the global impact of cAMP and its major effector mechanism, protein kinase A (PKA), on gene expression is not known. Here we show that treatment of wild-type S49 lymphoma cells for 24 h with 8-(4-chlorophenylthio)-cAMP (CPT-cAMP), a PKA-selective cAMP analog, alters the expression of ~4500 of ~13,600 unique genes. By contrast, gene expression was unaltered in Kin– S49 cells (that lack PKA) incubated with CPT-cAMP. Changes in mRNA and protein expression of several cell-cycle regulators accompanied cAMP-induced G1-phase cell-cycle arrest of wild-type S49 cells. Within 2 h, CPT-cAMP altered expression of 152 genes that contain evolutionarily conserved cAMP-response elements (CRE) within 5 kb of transcriptional start sites, including the circadian clock gene Per1. Thus, cAMP through its activation of PKA produces extensive transcriptional regulation in eukaryotic cells. These transcriptional networks include a primary group of CRE-containing genes and secondary networks that include the circadian clock. Keywords: time-course

2005-04-15 | GSE2413 | GEO

Transcription profiling of mouse S49 cells to study the global impact of cAMP and protein kinase A on gene expression

Project description:Although a substantial number of hormones and drugs increase cellular cAMP levels, the global impact of cAMP and its major effector mechanism, protein kinase A (PKA), on gene expression is not known. Here we show that treatment of wild-type S49 lymphoma cells for 24 h with 8-(4-chlorophenylthio)-cAMP (CPT-cAMP), a PKA-selective cAMP analog, alters the expression of ~4500 of ~13,600 unique genes. By contrast, gene expression was unaltered in Kin- S49 cells (that lack PKA) incubated with CPT-cAMP. Changes in mRNA and protein expression of several cell-cycle regulators accompanied cAMP-induced G1-phase cell-cycle arrest of wild-type S49 cells. Within 2 h, CPT-cAMP altered expression of 152 genes that contain evolutionarily conserved cAMP-response elements (CRE) within 5 kb of transcriptional start sites, including the circadian clock gene Per1. Thus, cAMP through its activation of PKA produces extensive transcriptional regulation in eukaryotic cells. These transcriptional networks include a primary group of CRE-containing genes and secondary networks that include the circadian clock.

2007-08-31 | E-GEOD-2413 | biostudies-arrayexpress

Transcriptome analysis of novel CPT-CEF-treated HT29 colon cancer cells to evaluate drug cytotoxicity

Project description:Purpose: To identify differentially expressed genes in HT29 colon cancer cells after treatment with a novel formulation of camptothecin with β-cyclodextrin-EDTA-Fe3O4 nanoparticle-conjugated nanocarriers (CPT-CEF) Methods:Treated HT29 cell lines with CPT-CEF, isolated total RNA from HT29 colon cancer cells, and prepared library for RNA sequencing. Carried out comparative transcriptomic studies between treated and untreated cells to find out which gene functions were dysregulated by CPT-CEF. Results: The study yielded 247 DEGs ((FDR<0.05, FC>2.0) that were affected by CPT-CEF treatment in the HT29 colon cancer cells. The results obtained from cell cycle analysis, mitochondrial depolarization assay and acridium orange/propidium iodide double staining showed potential of CPT-CEF in cancer cell inhibition. Conclusion: Our study successfully identified DEGs in the CPT-CEF treated HT29 colon cancer cells that pointed to inhibition of cancer progression. To further affirm, animal studies are needed.

2021-09-15 | GSE165875 | GEO

Transcription profiling of Zea mays embryos under camptothecin (CPT) treatment.

Project description:Camptothecin (CPT) is a plant alkaloid that specifically binds topoisomerase I (Topo I) inhibiting its activity and inducing double stranded breaks in the DNA, activating the genotoxic cell responses, and ultimately, it might trigger programmed cell death (PCD). We used microarrays to detail the changes in gene expression during as a consequence of CPT treatment in maize immature embryos. In four independent experiments immature embryos were plated on MS medium supplemented with 50 uM CPT and incubated during three days. Untreated embryos incubated on MS medium were used as controls.

2010-11-01 | E-MEXP-2702 | biostudies-arrayexpress

RNA_seq and Ribo_seq analyses of control and CPT-treated MCF7 cells

Project description:We used RNA-seq and Ribo-seq analyses to examine the effect of CPT treatment of translation efficiency (TE)

2017-04-01 | GSE96643 | GEO