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BET bromodomain inhibitors synergize with ATR inhibitors to induce DNA damage, apoptosis, senescence-associated secretory pathway and ER stress in Myc- induced lymphoma cells

ABSTRACT: The aim of the project was to determine the expression profiles of murine Myc-driven lymphpma cells (Lambda-820) treated with vehicle (DMSO, 1:1000), a BET inhibitor (RVX2135), an ATR inhibitor (VE-821) or a combination of RVX2135 and VE-821. All experimnets were performed in presence of 10uM Q-VD-OPH to block apoptosis. Cells were harvested 24 h after treatment start.

ORGANISM(S): Mus musculus

PROVIDER: GSE74873 | GEO | 2015/12/18

SECONDARY ACCESSION(S): PRJNA301706

REPOSITORIES: GEO

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BET bromodomain inhibitors synergize with ATR inhibitors to induce DNA damage, apoptosis, senescence-associated secretory pathway and ER stress in Myc- induced lymphoma cells

Project description:The aim of the project was to determine the expression profiles of murine Myc-driven lymphpma cells (Lambda-820) treated with vehicle (DMSO, 1:1000), a BET inhibitor (RVX2135), an ATR inhibitor (VE-821) or a combination of RVX2135 and VE-821. All experimnets were performed in presence of 10uM Q-VD-OPH to block apoptosis. Cells were harvested 24 h after treatment start. 4 samples (DMSO, RVX2135, VE-821 or RVX2135/VE-821) in duplicates

2015-12-18 | E-GEOD-74873 | biostudies-arrayexpress

ATR-mediated Proteome Remodeling is a Major Determinant of Homologous Recombination Capacity in Cancer Cells

Project description:DMSO or 5uM ATR inhibitor(VE-821) were treated for 8 days on U2OS cells prior to anlaysis.

2018-07-17 | PXD010223 | Pride

BET bromodomain inhibitors synergize with ATR inhibitors in melanoma.

Project description: Not available

| S-EPMC5596569 | biostudies-literature

Aldehyde dehydrogenase inhibitors promote DNA damage in ovarian cancer and synergize with ATM/ATR inhibitors.

Project description: Not available

| S-EPMC7914353 | biostudies-literature

Chemical Inhibitors of a Selective SWI/SNF Function Synergize with ATR Inhibition in Cancer Cell Killing.

Project description: Not available

| S-EPMC8273930 | biostudies-literature

MOLT-4 radiosensitization by VE-821

Project description:DNA damage induction by either radio- or chemo-therapy has been the most widely used approach in cancer therapy, exploiting the genomic instability of cancer cells. A promising strategy takes advantage of tumour specific abnormalities in DNA damage response. Inhibition of the ATR/Chk1 pathway has been shown to be synthetically lethal in cells with high levels of oncogene-induced replication stress and in p53- or ATM- deficient cells. In the presented study, we aimed to elucidate molecular mechanisms underlying radiosensitization of MOLT-4 cells by VE-821, a higly potent and specific inhibitor of ATR. We combined multiple approaches: cell biology techniques to reveal the inhibitor-induced phenotypes, and quantitative proteomics, phosphoproteomics, and metabolomics to comprehensively describe drug-induced changes in irradiated cells.

2018-07-16 | PXD008925 | Pride

Microarray analysis of HSVSMC treated with TGF-beta in the presence and absence of small molecule kinase inhibitors

Project description:Serum-starved, quieced HSVSMC (human saphenous vein smooth muscle cells, isolated from the great saphenous vein of coronary artery bypass graft patients) were treated with recombinant human TGFbeta-1 (10ng/mL) in the presence or absence of ALK5 kinase inhibitor SB-525334 (10uM) or ALK1/2 kinase inhibitor KO2288, https://doi.org/10.1371/journal.pone.0062721, (10uM). Gene expression analysis was performed on RNA extracted from cells at the 24h timepoint. RNA samples from three independent experiments (performed on cells from three different patients) were analysed. Quiesced, unstimulated cells were used as a negative control.

2019-08-16 | E-MTAB-7168 | biostudies-arrayexpress

Altering cancer transcriptomes using epigenomic inhibitors [Illumina beadchip]

Project description:We have compared the genome-wide effects on the transcriptome after treatment with ICG-001 (the specific CBP inhibitor) versus C646, a compound that competes with acetyl-coA for the Lys-coA binding pocket of both CBP and p300. We found that both drugs cause large-scale changes in the transcriptome of HCT116 colon cancer cells and PANC1 pancreatic cancer cells, and reverse some tumor-specific changes in gene expression. Interestingly, although the epigenetic inhibitors affect cell cycle pathways in both the colon and pancreatic cancer cell lines, the WNT signaling pathway was affected only in the colon cancer cells. Notably, WNT target genes were similarly down-regulated after treatment of HCT116 with C646 as with ICG-001. Total RNA obtained from isolated HCT116 or PANC1 cell lines were treated with 10uM ICG-001, 10uM C646, or 0.05% DMSO and collected after 12 or 96 hours.

2015-01-07 | E-GEOD-64038 | biostudies-arrayexpress

Quantitative proteomics of Giardia exposures to HKMT inhibitors

Project description:We explored differential protein expression (DEPs) during sublethal exposures of HKMT inhibitors (BIX-01294 = 10uM (B), Chaetocin = 20uM (C)) in log-phase (growth; TY) and encystation (differentiation; EC) at 8 and 24 hours relative to DMSO controls (D). In total, 18,527 peptides from 1,981 proteins in log-phase, and 19,852 peptides from 2,097 proteins were analysed in encysting cultures. In total, 56 proteins were up- and 36 down-regulated in log-phase trophozoites and 32 up- and 12 down during encystation upon BIX-01294-treatment relative to the DMSO controls. Following Chaetocin-treatment, 195 proteins were up- and 121 down-regulated in log-phase trophozoites, and 63 up- and 12 down during encystation. We have presented results by cell-phase given positive correlations were driven by culture condition and not between either Chaetocin or BIX-01294 inhibitor).

2020-08-04 | PXD016747 | Pride

mTOR inhibitors suppress homologous recombination repair and synergize with PARP inhibitors via regulating SUV39H1 in BRCA-proficient triple-negative breast cancer

Project description:This analysis was used to search for genes that were differentially expressed between cells treated with DMSO and those treated with the mTOR inhibitor everolimus.

2015-10-13 | GSE73923 | GEO

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