Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Gene expression profiling of isogenic malignant melanoma A375-BRAFV600E/NRASQ61 and A375-BRAFV600E/NRASQ61K cell lines

ABSTRACT: Gene expression profiling of isogenic malignant melanoma A375-BRAFV600E/NRASQ61 and A375-BRAFV600E/NRASQ61K cell lines

PROVIDER: PRJNA765441 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

Gene expression profiling of isogenic malignant melanoma A375-BRAFV600E/NRASQ61 and A375-BRAFV600E/NRASQ61K cell lines

Project description:BRAF-inhibitor (BRAFi)-resistance compromises long term survivorship of malignant melanoma patients, and mutant NRAS is a major mediator of BRAFi-resistance. We have employed NanoString nCounterTM transcriptomic analysis of isogenic human malignant melanoma cells that differ only by NRAS mutational status (BRAFi-sensitive A375-BRAFV600E/NRASQ61 versus BRAFi-resistant A375-BRAFV600E/NRASQ61K), identifying modulation of specific gene expression networks as a function of NRASQ61K-status.

2021-09-23 | GSE184633 | GEO

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

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

2014-05-20 | GSE42872 | GEO

Effect of PTEN knockout on dabrafenib-trametinib treatment in A375 melanoma cells - replicate 1

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. RNA sequencing and functional kinome analysis revealed the loss of PTEN led to an induction of FOXD3 and an increase in expression of the FOXD3 target gene, ERBB3/HER3. Inhibition of BRAFand MEK1/2 in PTEN null, BRAFV600E cells dramatically induced expression of ERBB3/HER3 relative to wild type cells. A synergy screen of epigenetic modifiers and kinase inhibitors in combination with inhibitors for mutant BRAF/MEK1/2 identified the pan ERBB/HER inhibitor, neratinib, as reversing the resistance observed in PTEN null, BRAFV600E cells. The findings indicate PTEN null BRAFV600E melanoma becomes dependent on ERBB/HER signaling when treated with clinically approved BRAF and MEK inhibitors. Future studies are warranted to test neratinib reversal of resistance in patient melanomas expressing ERBB3/HER3 in combination with its dimerization partner ERBB2/HER2.

2024-04-23 | PXD033866 | Pride

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

2024-04-23 | PXD033921 | Pride

Melanotransferrin (MELTF, MFI2, CD228) expression attenuates malignant melanoma progression in the A375-luc2 murine metastasis model and human patients

Project description:The cell-surface glycoprotein melanotransferrin (MELTF) is a member of the iron-binding transferrin superfamily expressed in human melanocytes and other cell types. Dysregulated MELTF-expression in malignant melanoma and other malignancies has been reported before but its specific role in melanomagenesis remains elusive. We performed CRISPR/Cas9-based MELTF deletion in human A375-luc2 malignant melanoma cells followed by transcriptomic analysis in order to explore the mechanistic role of MELTF in malignant melanoma.

2024-07-01 | GSE262543 | GEO

Homo sapiens strain:A375 BRAFV600E melanoma clones with acquired resistance to vemurafenib

Project description:Homo sapiens strain:A375 BRAFV600E melanoma clones with acquired resistance to vemurafenib

| PRJNA77989 | ENA

Neratinib, a Pan ERBB/HER Inhibitor, Restores Sensitivity of PTEN-null, BRAFV600E Melanoma to BRAF/MEK Inhibition

Project description:The A375, human BRAFV600E mutant melanoma, cell line (wildtype), two PTEN-null, BRAFV600E cell lines (KO5 and KO11), and PI3K overexpression cells (WT and PI3K H1047R mutant) were treated with small molecule inhibitors (dabrafenib, BRAF inhibitor; trametinib, MEK inhibitor alone and in combination for 0, 1 and 7 days

2019-04-27 | GSE130396 | GEO

Melanoma BRAFV600E induced proteome

Project description:By analyzing of the changes in proteome mediated by the oncogene BRAFV600E in melanoma cells we provide new insights on the pathways upregulated in these cells and possible new targets for therapy.

2018-06-25 | PXD008010 | Pride

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

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