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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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A375 melanoma cells treated with leflunomide 25uM

ABSTRACT: Human A375 melanoma cells were treated with leflunomide 25uM for 3 days, then RNA harvested 6 arrays

ORGANISM(S): Homo sapiens

SUBMITTER: Richard White

PROVIDER: E-GEOD-24526 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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DHODH modulates transcriptional elongation in the neural crest and melanoma.

White Richard Mark RM Cech Jennifer J Ratanasirintrawoot Sutheera S Lin Charles Y CY Rahl Peter B PB Burke Christopher J CJ Langdon Erin E Tomlinson Matthew L ML Mosher Jack J Kaufman Charles C Chen Frank F Long Hannah K HK Kramer Martin M Datta Sumon S Neuberg Donna D Granter Scott S Young Richard A RA Morrison Sean S Wheeler Grant N GN Zon Leonard I LI

Nature 20110301 7339

Melanoma is a tumour of transformed melanocytes, which are originally derived from the embryonic neural crest. It is unknown to what extent the programs that regulate neural crest development interact with mutations in the BRAF oncogene, which is the most commonly mutated gene in human melanoma. We have used zebrafish embryos to identify the initiating transcriptional events that occur on activation of human BRAF(V600E) (which encodes an amino acid substitution mutant of BRAF) in the neural cres ...[more]

PMID: 21430780

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A375 melanoma cells treated with leflunomide 25uM

Project description:Human A375 melanoma cells were treated with leflunomide 25uM for 3 days, then RNA harvested

2011-03-30 | GSE24526 | GEO

Homo sapiens

Project description:A375 melanoma cells treated with leflunomide 25uM

| PRJNA132661 | ENA

Transcriptome data from human malanoma A375 cells stably expressing MAP4K5 shRNA.

Project description:MAP4K5 is serine/threonine protein kinase similar to yeast SPS1/STE20 kinase. MAP4K5 activates JNK in mammalian cells, which suggests a role in stress response. MAP4K5 is involved in immune functions. We used microarray to investigate genome-wide transcriptional change from MAP4K5 knockdown in A375 cells. Total RNA's from the A375 cells where MAP4K5 was stably knocked down by shRNA were analyzed. As a control, RNA's from A375 cells were also analyzed.

2014-09-18 | E-GEOD-61497 | biostudies-arrayexpress

Analysis of A375 and A375 clones that acquired resistance to GSK2118436 after treatment with GSK2118436 (GSK436), GSK1120212 (GSK212), or the combination of GSK2118436 and GSK1120212 for 24 hour

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.

2012-02-01 | E-GEOD-35230 | biostudies-arrayexpress

Expression data of A375 melanoma cells after DMSO or MLN4924 treatment from 1 hour to 24 hour

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

Expression data of A375 melanoma cells after DMSO or MLN4924 +/- Nutlin treatment for 26 hours

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

RNA-seq of human melanoma cancer cell line A375 treated with BET inhibitor JQ1 against untreated control

Project description:To set the relevance of BRD4 as repressor, we performed gene expression profile by RNA-seq in A375 treated with BETi JQ1 to identify potential BRD4 target genes.

2021-03-31 | E-MTAB-8649 | biostudies-arrayexpress

Gene expression profile in A375 melanoma cells after 45 functionally important molecules were knocked down using siRNA

Project description:Affymetrix microarray data were generated from A375 melanoma cells treated in vitro with siRNAs against 45 transcription factors and signalling molecules. 45 functionally important molecules were knocked down in A375 melanoma cells by siRNA. Then the gene expression profiles of these A375 cells, along with untreated cells and sRNA control treated cells were analysed by microarrays.

2012-03-15 | E-GEOD-31534 | biostudies-arrayexpress

Expression data from BRAFV600E A375 melanoma cells treated with vehicle or vemurafenib

Project description:Vemurafenib is a BRAF inhibitor with specificity for the most common BRAF mutant encountered in melanomas (BRAFV600E). Vemurafenib suppresses the proliferation of BRAF mutant human melanoma cells by suppressing downstream activation of the MEK/ERK mitogen activated protein kinases. We used microarrays to examine the transcriptional response of a vemurafenib-sensitive BRAFV600E human melanoma cell line (A375) to vemurafenib in order to further delineate the mechanisms by which BRAFV600E drives cell proliferation and energy metabolism in human melanoma. BRAFV600E A375 human melanoma cells were treated with vehicle (0.1% DMSO) or 10 uM vemurafenib for 24 h after which total RNA was extracted. Cells were prepared and RNA was extracted in 3 separate batches (three different cell stocks on three separate days) providing three independent replicates (n=3). Paired replicates (prepared from the same stock of cells on the same day) are denoted by A, B and C.

2014-05-20 | E-GEOD-42872 | biostudies-arrayexpress

Microarray gene expression analysis of human melanoma A375 cells treated with 0.5mM phenformin against untreated control

Project description:The aim of this study was to characterize the effect of phenformin on human melanoma cells at the transcritpional level. Experimentally, A375 cells have been treated or untreated with 0.5mM phenformin for 72h, then lysed for RNA isolation.

2018-11-01 | E-MTAB-6665 | biostudies-arrayexpress

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