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

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

SUBMITTER: Liao H

PROVIDER: S-ECPF-GEOD-30531 | biostudies-other | 2011 Nov

REPOSITORIES: biostudies-other

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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

2011-07-09 | GSE30531 | GEO

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

| S-ECPF-GEOD-39091 | biostudies-other

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

2012-07-04 | GSE39091 | GEO

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

2012-07-03 | E-GEOD-39091 | 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.

| S-ECPF-GEOD-42872 | biostudies-other

Acid ceramidase expression modulates the sensitivity of A375 melanoma cells to dacarbazine.

Project description:Dacarbazine (DTIC) is the treatment of choice for metastatic melanoma, but its response in patients remains very poor. Ceramide has been shown to be a death effector and to play an important role in regulating cancer cell growth upon chemotherapy. Among ceramidases, the enzymes that catabolize ceramide, acid ceramidase (aCDase) has been implicated in cancer progression. Here we show that DTIC elicits a time- and dose-dependent decrease of aCDase activity and an increase of intracellular ceramide levels in human A375 melanoma cells. The loss of enzyme activity occurred as a consequence of reactive oxygen species-dependent activation of cathepsin B-mediated degradation of aCDase. These events preceded autophagic features and loss of cell viability. Down-regulation of acid but not neutral or alkaline ceramidase 2 resulted in elevated levels of ceramide and sensitization to the toxic effects of DTIC. Conversely, inducible overexpression of acid but not neutral ceramidase reduced ceramide levels and conferred resistance to DTIC. In conclusion, we report that increased levels of ceramide, due to enhanced degradation of aCDase, are in part responsible for the cell death effects of DTIC. These results suggest that down-regulation of aCDase alone or in combination with DTIC may represent a useful tool in the treatment of metastatic melanoma.

| S-EPMC3151065 | biostudies-literature

Gene expression profiling in anchorage-independent melanoma A375 cells

Project description:Analysis of gene expression and compare the significant changed genes with associated phenotypes Total RNA extracted from adherent and suspension culture of A375 cells

| S-ECPF-GEOD-42876 | biostudies-other

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.

| S-ECPF-GEOD-35230 | biostudies-other

A3 adenosine receptors modulate hypoxia-inducible factor-1alpha expression in human A375 melanoma cells.

Project description:Hypoxia-inducible factor-1 (HIF-1) is a key regulator of genes crucial to many aspects of cancer biology. The purine nucleoside, adenosine, accumulates within many tissues under hypoxic conditions, including that of tumors. Because the levels of both HIF-1 and adenosine are elevated within the hypoxic environment of solid tumors, we investigated whether adenosine may regulate HIF-1. Here we show that, under hypoxic conditions (< 2% O2), adenosine upregulates HIF-1alpha protein expression in a dose-dependent and time-dependent manner, exclusively through the A3 receptor subtype. The response to adenosine was generated at the cell surface because the inhibition of A3 receptor expression, by using small interfering RNA, abolished nucleoside effects. A3 receptor stimulation in hypoxia also increases angiopoietin-2 (Ang-2) protein accumulation through the induction of HIF-1alpha. In particular, we found that A3 receptor stimulation activates p44/p42 and p38 mitogen-activated protein kinases, which are required for A3-induced increase of HIF-1alpha and Ang-2. Collectively, these results suggest a cooperation between hypoxic and adenosine signals that ultimately may lead to the increase in HIF-1-mediated effects in cancer cells.

| S-EPMC1502026 | biostudies-literature

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