Expression data of A375 melanoma cells after DMSO or MLN4924 treatment from 1 hour to 24 hour
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE30531 | GEO | 2011/07/09
SECONDARY ACCESSION(S): PRJNA143311
REPOSITORIES: GEO
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Project description:Microarrays were used to determine the change in gene expression of genes involved in the CDT1/NAE pathway A375 cells were grown and then incubated in the presence of either DMSO as control or 650nM MLN4924. Cells were treated for 1, 2, 4, 8, and 24 hours. RNA extraction and hybridization on Affymetrix HG-U133Plus 2.0 arrays were performed.
2011-07-09 | E-GEOD-30531 | biostudies-arrayexpress
Project description:Microarrays were used to determine the change in gene expression of genes involved in the CDT1/NAE pathway A375 cells were grown and then incubated in the presence of either DMSO as control or 650nM MLN4924. Cells were treated for 1, 2, 4, 8, and 24 hours. RNA extraction and hybridization on Affymetrix HG-U133Plus 2.0 arrays were performed.
| S-ECPF-GEOD-30531 | biostudies-other
Project description:Microarrays were used to determine the change in gene expression of genes involved in the p53 pathway after siRNA knock down of p53, CDT1 or BRCA1 A375 cells were grown, transfected with siRNA, incubated for 48hrs, then incubated for another 26hrs in the presence of either 0.065% DMSO as control, 650nM MLN4924, 5uM Nutlin or 100nM Daunorubicin. RNA extraction and hybridization on Affymetrix HG-U133Plus 2.0 arrays were performed.
2012-07-04 | GSE39091 | GEO
Project description:Microarrays were used to determine the change in gene expression of genes involved in the p53 pathway after siRNA knock down of p53, CDT1 or BRCA1 A375 cells were grown, transfected with siRNA, incubated for 48hrs, then incubated for another 26hrs in the presence of either 0.065% DMSO as control, 650nM MLN4924, 5uM Nutlin or 100nM Daunorubicin. RNA extraction and hybridization on Affymetrix HG-U133Plus 2.0 arrays were performed. 12 conditions in triplicate for a total of 42 samples
2012-07-03 | E-GEOD-39091 | biostudies-arrayexpress
Project description:Microarrays were used to determine the change in gene expression of genes involved in the p53 pathway after siRNA knock down of p53, CDT1 or BRCA1 A375 cells were grown, transfected with siRNA, incubated for 48hrs, then incubated for another 26hrs in the presence of either 0.065% DMSO as control, 650nM MLN4924, 5uM Nutlin or 100nM Daunorubicin. RNA extraction and hybridization on Affymetrix HG-U133Plus 2.0 arrays were performed. 12 conditions in triplicate for a total of 42 samples
| S-ECPF-GEOD-39091 | biostudies-other
Project description:In an effort to understand the mechanisms of acquired resistance to BRAF inhibitors, we isolated clones that acquired resistance to the BRAF inhibitor GSK2118436 derived from the A375 BRAF V600E mutant melanoma cell line. This resistance clones acquired mutations in NRAS and MEK1. One clones, 16R6-4, acquired two mutations in NRAS – Q61K and A146T. Proliferation and western blot analyses demonstrated that these clones were insensitive to single agent GSK2118436 or GSK1120212 (an allosteric MEK inhibitor) but were sensitive to the combination of GSK2118436 and GSK1120212. To further characterize this combination, global transcriptomic analysis was performed in A375 and 16R6-4 after 24 hour treatment with GSK2118436, GSK1120212 or the combination of GSK2118436 and GSK1120212. This data set was published in Molecular Cancer Therapeutics with the title “Combined inhibition of BRAF and MEK, BRAF and PI3K/mTOR, or MEK and PI3K/mTOR overcomes acquired resistance to the BRAF inhibitor GSK2118436, mediated by NRAS or MEK mutations” by Greger, J.G., et.al. A375 and 16R6-4 (an A375 derived GSK2118436 resistance clone) were treated for 24 hours with 0.1 micromolar GSK2118436, 1 micromolar GSK2118436, 0.01 micromolar GSK1120212, 0.1 micromolar GSK2118436 + 0.01 micromolar GSK1120212, or 1 micromolar GSK2118436 + 0.01 micromolar GSK1120212.
| S-ECPF-GEOD-35230 | biostudies-other
Project description:In an effort to understand the mechanisms of acquired resistance to BRAF inhibitors, we isolated clones that acquired resistance to the BRAF inhibitor GSK2118436 derived from the A375 BRAF V600E mutant melanoma cell line. This resistance clones acquired mutations in NRAS and MEK1. One clones, 16R6-4, acquired two mutations in NRAS – Q61K and A146T. Proliferation and western blot analyses demonstrated that these clones were insensitive to single agent GSK2118436 or GSK1120212 (an allosteric MEK inhibitor) but were sensitive to the combination of GSK2118436 and GSK1120212. To further characterize this combination, global transcriptomic analysis was performed in A375 and 16R6-4 after 24 hour treatment with GSK2118436, GSK1120212 or the combination of GSK2118436 and GSK1120212. This data set was published in Molecular Cancer Therapeutics with the title “Combined inhibition of BRAF and MEK, BRAF and PI3K/mTOR, or MEK and PI3K/mTOR overcomes acquired resistance to the BRAF inhibitor GSK2118436, mediated by NRAS or MEK mutations” by Greger, J.G., et.al.
2012-02-01 | GSE35230 | GEO
Project description:Acquired drug tolerance has been a major challenge in cancer therapy. Recent evidence has revealed the existence of slow-cycling persister cells that survive drug treatments and give rise to multi-drug-tolerant mutants in cancer. Cells in this dynamic persister state can escape drug treatment by undergoing various epigenetic changes, which may result in a transient metabolic rewiring. In this study, with the use of untargeted metabolomics and phenotype microarrays, we characterize the metabolic profiles of melanoma persister cells mediated by treatment with vemurafenib, a BRAF inhibitor. Our findings demonstrate that metabolites associated with phospholipid synthesis, pyrimidine, and one-carbon metabolism and branched-chain amino acid metabolism are significantly altered in vemurafenib persister cells when compared to the bulk cancer population. Our data also show that vemurafenib persisters have higher lactic acid consumption rates than control cells, further validating the existence of a unique metabolic reprogramming in these drug-tolerant cells. Determining the metabolic mechanisms underlying persister cell survival and maintenance will facilitate the development of novel treatment strategies that target persisters and enhance cancer therapy.
| S-EPMC8619236 | biostudies-literature
Project description:Actin is a highly conserved protein that is expressed in all eukaryotic cells and has essential functions in the cytoplasm and the nucleus. Nuclear actin is involved in transcription by all three RNA polymerases, chromatin remodelling, RNA processing, intranuclear transport, nuclear export and in maintenance of the nuclear architecture. The nuclear actin level and polymerization state are important factors regulating nuclear processes such as transcription. Our study shows that, in contrast to the cytoplasm, the majority of endogenous nuclear actin is unpolymerized in human melanoma A375 cells. Most mammalian cells express the two non-muscle ?- and ?-actin isoforms that differ in only four amino acids. Despite their sequence similarity, studies analysing the cytoplasmic functions of these isoforms demonstrated that ?- and ?-actins show differences in localization and function. However, little is known about the involvement of the individual actin isoforms in nuclear processes. Here, we used the human melanoma A375 cell line to analyse actin isoforms in regard to their nuclear localization. We show that both ?- and ?-non-muscle actin isoforms are present in nuclei of these cells. Immunolocalization studies demonstrate that both isoforms co-localize with RNA polymerase II and hnRNP U. However, we observe differences in the ratio of cytoplasmic to nuclear actin distribution between the isoforms. We show that ?-actin has a significantly higher nucleus-to-cytoplasm ratio than ?-actin.
| S-EPMC4628621 | biostudies-literature
Project description:BackgroundMonitoring salt consumption in children is essential for informing and implementing public health interventions to reduce children's salt intake. However, collection of 24-hour urines, considered as the most reliable approach, can be especially challenging to school children. This study aimed to assess the agreement between 24-hour urine (24hrU) and 24-hour food recall (24hrFR) in: (1) estimating salt intake in children; (2) classifying salt intakes above the recommended upper level set for children, and; (3) estimating change in mean salt intake over time.MethodsThis study utilised data from two cross-sectional surveys of school children aged 8 to 12 years living in the state of Victoria, Australia. A single 24hrU and 24hrFR were collected from each participant. Suspected inaccurate urine collections and implausible energy intakes were excluded based on pre-defined criteria. The agreement between the two methods was assessed using Bland-Altman methodology, the intraclass correlation coefficient (ICC), and the kappa statistic. The difference between the measured change in salt intake over time using 24hrU and 24hrFR was derived using mixed effects linear regression analysis.ResultsA total of 588 participants provided a 24hrU and 24hrFR. Overall, there was no meaningful difference in mean estimated salt intake between the two methods (- 0.2 g/day, 95% CI - 0.5 to 0.1). The Bland-Altman plot showed wide 95% limits of agreement (- 7.2 to 6.8). The ICC between the two methods was 0.13 (95% CI 0.05 to 0.21). There was poor interrater reliability in terms of classifying salt intake above the recommended upper level for children, with an observed agreement of 63% and kappa statistic of 0.11. The change in mean salt intake over time was 0.2 g/day (- 0.4 to 0.7) based on 24hrU, and 0.5 g/day (- 0.0 to 1.1) based on 24hrFR, with a difference-in-differences of 0.4 g/day (- 0.3 to 1.1).Conclusions24hrFR appears to provide a reasonable estimate of mean salt intake as measured by 24hrU in Australian school children. However, similar to previous observations in adults, and of studies exploring other alternative methods for estimating salt intake, 24hrFR is a poor predictor of individual-level salt intake in children.
| S-EPMC9664040 | biostudies-literature