Project description:We treated steroid-deprived MCF7 cells with DMSO (Vehicle), 1 nM 17b-estradiol (E2), 100 nM fulvestrant (Fulv), or a combination of fulvestrant and estradiol for 24 hours
Project description:Primary lung fibroblasts were grown to confluence in DMEM 10% FBS, serum starved in DMEM 0.5% FBS for 18 hours. Cells were then treated in the presence or absence of 100 nM ET-1 in the same medium for an additional 4 hours. Keywords: repeat sample
Project description:primary lung fibroblasts p3 from normal periphery of resected cancer. grown in DMEM 10% FBS, until confluence, then DMEM 0.5% FBS for 18 hours. Media were then changed and incubated for an additional 4 hours in the presence or absence of 100 nM endothelin-1. Data represent two independent experiments performed on two different occasions. Keywords: other
Project description:NCI-H2030 lines were seeded in 6-well plates in complete culture medium and cultured at densities allowing exponential growth: 50000 cells/well. After 24 h, compounds were added (DMOS, adagrasib (30 nM), K-975 (100 nM) and adagrasib (30 nM)+K-975 (100 nM)) at a final percentage of 0.2% DMSO. Twenty-four hours after compounds addition, cells were used for transcriptomic profiling.
Project description:Analysis of Human bone mesenchymal stem cells treated separately with DMSO vehicle, 100 nM perfluorooctanesulfonat(PFOS), 100 nM perfluorooctanoic acid(PFOA), 100 nM perfluorohexanesulphonate(PFHxS) or100 nM Chlorinated polyfluoroalkyl ether sulfonate(F-53B) for 7 days. Results provide insight into the molecular mechanisms by which PFASs interfere with osteogenic differentiation potential in HBMSCs.
Project description:FGFR1-amplified lung cancer cell line NCI-H1581 was treated with FGFR inhibitor AZD4547 (0.1μM) or DMSO vehicle for 24 hours. Then TMT-labeled mass spectrometry-based proteomics was carried out in cell lysates to analyze the differentially expressed proteins between two groups.
Project description:Cells expressing mutant huntingtin were treated in triplicate with serum-free DMEM with vehicle (Q111SST) or serum-free DMEM with one of 4 protective compounds (Cyproheptadine, Loxapine, Diacylglycerol Kinase Inhibitor II, Meclizine) for 24 hours. Wild type cells were also treated with serum-free DMEM with vehicle (Q7SST) as an additional control for 24 hours. We examined the compounds' proteomic and some phosphoproteomic effects on the cells using shotgun proteomics.
Project description:The mammalian target of rapamycin (mTOR) is a central regulator of cell proliferation. Inhibitors of mTOR are being evaluated as anti-tumor agents. Given the emerging role of microRNAs (miRNAs) in tumorgenesis we hypothesized that miRNAs could play important roles in the response of tumors to mTOR inhibitors. Rapamycin resistant myogenic cells developed by long-term rapamycin treatment showed extensive reprogramming of miRNAs expression, characterized by up-regulation of the mir-17~92 and related clusters and down-regulation of tumor-suppressor miRNAs. Antagonists of oncogenic miRNA families and mimics of tumor suppressor miRNAs (let-7) restored rapamycin sensitivity in resistant tumor cells. This study identified miRNAs as new downstream components of the mTOR-signaling pathway, which may determine the response of tumors to mTOR inhibitors. Total RNA extraction and hybridization on Affymetrix microarrays of rapamycin sensitive (RS) cells (BC3H1, mouse brain tumor cell line with myogenic properties, ATCC) cultured in Dulbecco’s modified essential medium (DMEM) media supplemented with 20% fetal bovine serum (FBS), penicillin (100 U/ml) and streptomycin (100 mg/ml). Rapamycin resistant cells (RR1) were developed by culturing BC3H1 cells in the presence of 1 uM rapamycin for 6 months. Three samples in triplicates: 1) Rapamycin sensitive cells treated with DMSO for 24 h(BC3H1, reference), 2) Rapamycin sensitive cells treated for 24 h with 100 nM rapamycin (BC3H1+R), 3) Rapamycin resistant cells constantly treated with 1uM Rapamycion (RR1+R).
Project description:SW480 cells overexpressing BOP1, CKS2 or NFIL3 migrated more actively compared to Control cells. Migration induced by BOP1, CKS2 or NFIL3 was repressed by interfering with distinct signaling systems using small- molecular-weight inhibitors, i.e., interference with PI3K, JNK and Notch in the case of BOP1, with PI3K and p38 MAPK in the case of CKS2, as well as with PI3K, p38 and mTOR in the case of NFIL3. Gene expression profilings suggest that BOP1, CKS2 and NFIL3 overexpression are associated functionally with a series of migration-related genes, which can be repressed transcriptionally by specific pathway inhibitors. SW480 stable cells were grown in DMEM, 10% FCS, and treated for 24 hr with the following inhibitors or with solvent (DMSO): SW480_Control with DMSO; SW480_BOP1 with DMSO, LY294002 (3.3 uM), SP600125 (33.3 nM) and DAPT (667 nM); SW480_CKS2 with DMSO, LY294002 (3.3 uM) and SB203580 (3.3 uM); SW480_NFIL3 with DMSO, LY294002 (3.3 uM), SB203580 (3.3 uM) and Rapamycin (33.3 nM).
Project description:A toxicogenomics approach was used to qualitatively and quantitatively compare gene expression changes in rat primary hepatocytes exposed to 2,3,4,7,8-pentachlorodibenzofuran (4-PeCDF) or 2,3,7,8-tetrachlorodibenzofuran (TCDF). Hepatocytes from five individual rats were exposed for 24 hours to 11 concentrations of each chemical ranging from 0.00001 nM to 100 nM and a vehicle control.