Browse
Submit Data
Databases
API
Help

Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

RNAseq of A375 melanoma cells and A375 with ARID1A KO in control conditions and treatment with trametinib, vemurafenib or combination

ABSTRACT: The experiment aimed to study mechanisms of melanoma drug resistance. ARID1A confers resistance to trametinib and therefore RNAseq was collected alongside other omics data for parental A375 likes, and A375 lines with ARID1A KO, in the presence of no drug, trametinib, vemurafenib or their combination

INSTRUMENT(S): NextSeq 2000

ORGANISM(S): Homo sapiens

SUBMITTER:

PROVIDER: E-MTAB-14759 | biostudies-arrayexpress |

SECONDARY ACCESSION(S): ERP168497

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

RNAseq of A375 melanoma cells and A375 with ARID1A KO in control conditions and treatment with trametinib, vemurafenib or combination

Project description:RNAseq of A375 melanoma cells and A375 with ARID1A KO in control conditions and treatment with trametinib, vemurafenib or combination

| PRJEB85066 | ENA

Effect of PTEN knockout on dabrafenib-trametinib treatment in A375 melanoma cells - replicate 2

Project description:Approximately 50% of melanomas harbor an activating BRAFV600E mutation. Standard of care involves a combination of inhibitors targeting mutant BRAF and MEK1/2, the substrate for BRAF in the MAPK pathway. PTEN loss of function mutations occur in 40% of BRAFV600E melanomas, resulting in increased PI3K/AKT activity that enhances resistance to BRAF/MEK combination inhibitor therapy. To compare the response of PTEN null to PTEN wild type cells in an isogenic background, CRISPR was used to knock out PTEN in the A375 melanoma cell line that harbors a BRAFV600E mutation. Kinome profiling was performed using the parental line and two PTEN KO clones (5 and 11), treated with DMSO, or treated with 100nM dabrafenib and 10nM trametinib for 1 day or for 7 days. PTEN KO cells showed dramatically increased binding of HER3 and AKT3 compared to wild type. The activation of the SOX10-FOXD3-HER3-AKT axis in PTEN KO cells could be targeted with the ERBB/HER inhibitor neratinib.

2024-04-23 | PXD033921 | Pride

Homo sapiens strain:A375

Project description:CRISPR/Cas9 drug uptake screen in A375

| PRJNA416669 | ENA

Whole Exome PC9 and A375

Project description:Drug resistant population of PC9(human non-small cell lung cancer) or A375 (human melanoma) cell lines were used for this study. By exome sequencing, we will analyse mutations of cells in drug tolerent state and after drug holiday.

| EGAS00001002493 | EGA

Response and resistance of low grade ovarian cancer cells to trametinib

Project description:HOC-7 and MPSC1 are low grade serous ovarian cancer cell lines. These cells was treated with different doses of trametinib in an attempt to identify biomarkers that can be used to predict chemoresponse to this drug. We used microarrays to identify genes induced by trametinib.

2020-04-15 | GSE148648 | GEO

Expression data from A375 melanoma parental and persister cells

Project description:Identify transcriptionnally and translationally regulated mRNA in melanoma parental and persister cells In this dataset, we include expression data of A375 melanoma drug-naïve parental cells and A375 melanoma persister cells that survived from BRAF and MEK inhibition. The expression data are studied in both total RNA and polysome-bounded RNA.

2019-09-20 | GSE137724 | GEO

Transcriptomic analysis of trametinib-resistant HCT116 colorectal carcinoma cells compared to the parental control cells

Project description:HCT116 cells were treated with with increasing concentrations of trametinib over 2 months. Drug-resistant clones emerged and were cultured in the presence of 30 nmol/L trametinib. These cells exhibited a greater than 10-fold increase in the GI50 for trametinib compared to the parental cell line. RNA-seq of the resistant clone HCT116_R4 versus the parental cells identified differentially expressed genes potentially involved in resistance.

2018-10-23 | GSE118490 | GEO

Human A375 melanoma cell line treated with ciclopirox and crizotinib

Project description:To generate drug signatures in human A375 melanoma cell lines. A375 cell line was plated at 4 x 105 cells/mL overnight and treated with ciclopirox or crizotinib at 75% inhibitory concentrations (IC75, determined previously at 72h of treatment) or DMSO (vehicle) for 8h or 24h before harvest.

2018-01-01 | GSE59340 | GEO

The geroprotectors trametinib and rapamycin combine additively to extend mouse healthspan and lifespan

Project description:Suppression of the insulin-IGF-mTORC1-Ras network ameliorates aging in animals. Many drugs have targets in the network because of its roles in cancer and metabolic disease and are candidates for repurposing as geroprotectors. Rapamycin, an established geroprotective drug, blocks mTORC1 signaling, and trametinib inhibits the Ras-MEK-ERK pathway. In this study, we assessed survival and health of male and female mice treated with trametinib, rapamycin or their combination. We show here that trametinib treatment extended lifespan in both sexes and that its combination with rapamycin was additive. Combination treatment reduced liver tumors in both sexes and spleen tumors in male mice, blocked the age-related increase in brain glucose uptake and strongly reduced inflammation in brain, kidney, spleen and muscle and circulating levels of pro-inflammatory cytokines. We conclude that trametinib is a geroprotector in mice and that its combination with rapamycin is more effective than either drug alone, making the combination a candidate for repurposing as a gerotherapy in humans.

2025-03-27 | GSE288795 | GEO

Rosiglitazone and Trametinib to treat basal bladder tumors [ATAC-Seq]

Project description:To investigate the anti-tumor effect of Rosiglitazone+Trametinib in basal bladder cancer, we tested the drug combination in BBN-induced basal tumor mouse model in vivo and BBN-derived tumor cell line BBN963 in vitro.

2024-03-15 | GSE234325 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data