Similar Datasets
Project description:Glioblastoma cells were treated with vehicle (DMSO) or mepazine (MPZ, 20 μM, 4 hours) and prepared for RNAseq according to ActiveMotif standard procedure. The list of differentially expressed genes from DESeq2 output was selected based on 10% adjusted p-value level and FDR of 0.1.
2019-10-18 | GSE139018 | GEO
Project description:The influences of 40 hours treatment of 30 μM chrysin (CAS No: 480-40-0) or 30 μM nifurtimox (CAS No: 23256-30-6) on A549 cell gene expression profile were examined by RNA sequencing.
2022-03-01 | GSE193541 | GEO
Project description:We sought to identify pathways dysregulated in Mycobacterium tuberculosis upon treatment with the compound C10. We treated M. tuberculosis with DMSO, 5 μM C10, or 25 μM C10 for 48 hours in Sauton's medium and used RNA-sequencing to compare transcriptional profiles.
2019-05-31 | GSE129833 | GEO
Project description:Background: The receptor tyrosine kinase (RTK) EGFR is overexpressed and mutated in NSCLC. These mutations can be targeted by RTK inhibitors (TKIs) such as erlotinib. Chromatin-modifying agents may offer a novel therapeutic approach by sensitizing tumor cells to TKIs. Methods: The NSCLC cell lines HCC827 (EGFR mutant, adenocarcinoma), A549 (EGFR wt, adenocarcinoma) andNCI-H460 (EGFR wt, large cell carcinoma) were analyzed by SNP6.0 array. Changes in proliferation after panobinostat (LBH-589, PS) and erlotinib treatment were quantified by WST-1 assay and apoptosis by Annexin V/7-AAD flow cytometry. Abundance of target proteins and histone marks (acH3, H3K4me1/2/3) was determined by immunoblotting. Results: As expected, the EGFR wt cell lines A549 and NCI-H460 were quite insensitive to the growth-inhibitory effect of single-agent erlotinib (IC50 70-100 μM), compared to HCC827 (IC50 < 0.02 μM). PS treatment diminished growth to <50 % in both EGFR wt cells, and <30 % in HCC827. The combination of both drugs reduced proliferation by >95 % in HCC827, ≥70 % in A549, but not further in NCI-H460. PS alone induced differentiation and expression of p21WAF1/CIP1 and p53 and decreased CHK1 in all three cell lines, with almost no further effect when combined with erlotinib. In contrast, combination treatment additively decreased pEGFR, pERK, pAKT in A549, and synergistically induced acH3 in both adenocarcinoma lines. Surprisingly, we saw an induction of H3K4 methylation marks after erlotinib treatment in HCC827 (and to a lesser extent in A549) that was even further enhanced by combination with PS. Conclusion: We were able to show that PS synergistically sensitized lung adenocarcinoma cells to the antiproliferative effects of erlotinib. Since single-agent erlotinib has only modest clinical effects in lung adenocarcinoma EGFR wt patients, its combination with an HDACi might offer a promising therapy approach.
2014-12-03 | GSE63784 | GEO
Project description:Human melanoma cell line A375 and A2058 were incubated with DMSO (control group) or Vemurafenib (1 μM in DMSO) for 72 hours. Total RNA was isolated with Qiagen RNA isolation kit; 1.5 μg of total RNA was used as template for cDNA synthesis.
2015-12-02 | GSE52882 | GEO
Project description:To study the impact of TGF signaling on the transcriptome of vascular smooth muscle cells, we cultured human umbilical artery smooth muscle cells as 3D aggregates in hanging drops for 48 hours. One group was treated with TGFβRI/II inhibitor LY2109761 (10 μM, additional 10 μM after 24 h), the other group with solvent (DMSO) as control. RNA was isolated from both groups after 48h
2019-12-16 | GSE133649 | GEO
Project description:In this study, we used quantitative proteomics mass spectrometry with 16-plex TMT labeling to compare individual protein levels of DMSO and 1 μM CSN5i-3-treated K562 cells for 2, 8, and 24 hours. CSN5i-3 is a selective and potent inhibitor of Cop9 Signalosome (CSN), which regulates the activity of Cullin-RING E3 ubiquitin ligases (CRLs). CSN5i-3 treatment resulted in reduced CSN activity, and consequently increased cullin neddylation and constitutively active CRL. Gene Ontology analysis of the changed proteins between DMSO- and CSN5i-3-treated samples showed the enrichment of CSN subunits, cell cycle and chromosome-related components, and phosphatase complex, which include multiple CSN subunits (e.g., CSN7B and CSN5), components of CRLs, especially CRL SRs (e.g., SKP2, ELOA and DCAF1/VPRBP), and known substrates of CRLs (e.g., MAGEA6, GLUL, and RHOB). Indeed, eight out of the top 20 most decreased proteins were CRL adaptor and substrate receptors, two out of the top 20 were E2 proteins (CDC34/UBE2R1 and UBE2R2), and two were CSN subunits. Eight out of the top 20 most increased proteins were reported CRL substrates.
2022-09-05 | PXD027862 | Pride
Project description:Baicalein, a purified flavonoid compound with defined chemical structure extracted from the dry roots of Scutellaria radix that is a broadly used herb in China, has been proved to possess significant anti-hepatoma activity by inhibiting cell proliferation, invasion, metastasis and inducing apoptosis, autophagy via several cancer-related signaling molecules. In recent years, emerging studies have demonstrated that Chinese medicinal herbs can exert their anti-tumor effects through targeting lncRNAs，such as curcumin, camptothecin, resveratrol，paclitaxel. However, there is still no related report about the effects of baicalein on lncRNA expression profile when it exerts its inhibition on hepatoma tumor growth. To investigate whether the antitumor effect of baicalein is related to its modulation of lncRNA expression in hepatocellular carcinoma (HCC), we profiled the lncRNA expression in HCC cell line Bel-7402 treated with baicalein (0, 40, 80μM) for 24 hours using lncRNA microarray and detected the changes by comparing the lncRNA expression profile of HCC cell line Bel-7402 treated with baicalein (40 and 80 μM) and its DMSO control (0 μM). These findings suggest that modulation of lncRNA expression may be an important mechanism underlying the anti-hepatoma effects of baicalein and lay the groundwork for further investigations. To investigate whether the antitumor effect of baicalein is related to its modulation of lncRNA expression in hepatocellular carcinoma (HCC), we profiled the miRNA expression in HCC cell line Bel-7402 treated with baicalein (0, 40, 80μM) for 24 hours using miRNA microarray and detected the changes by comparing the lncRNA expression profile of HCC cell line Bel-7402 treated with baicalein (40 and 80 μM) and its DMSO control (0 μM). These findings suggest that modulation of lncRNA expression may be an important mechanism underlying the anti-hepatoma effects of baicalein and lay the groundwork for further investigations.
2018-03-01 | GSE95504 | GEO
Project description:In vitro genomic analyses of clozapine response. Genome wide gene expression profiling was performed across several experimental conditions of clozapine exposure. LCLs were exposed for 24 hours to 1x, 10x, 50x and 100x clinical concentration (2μM, 20μM,100μM,200 μM clozapine) and vehicle (DMSO); each concentration was measured in 4 cell lines.
2020-10-01 | GSE158819 | GEO
Project description:To examine the potential mechanism of anlotinib to inhibit intrahepatic cholangiocarcinoma, we used RNA-seq to analyze the effect of anlotinib treatment on the transcriptome changes of intrahepatic cholangiocarcinoma cell lines HCCC9810 and RBE. HCCC9810 and RBE cells were treated with DMSO or anlotinib at 5 μM for 24 hours, and then subjected to total RNA isolation and deep sequencing. We used Venn diagrams of RNA-seq results of HCCC9810 and RBE cells treated with anlotinib to indicate genes that were up- or down-regulated (adjusted P value <0.05, fold = 2.0). There are 420 genes in both groups (Figure 4A, 273 genes up-regulated and 147 genes down-regulated). In summary, the above sequencing results were analyzed by bioinformatics, and it was concluded that by inactivating the VEGF / PI3K / AKT signaling pathway and through cell cycle arrest, anlotinib treatment inhibited the proliferation and invasion of tumor cells and promoted Apoptosis.
2021-05-01 | GSE149901 | GEO