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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Whole-exome sequencing of genomic DNA from patient-derived melanoma cell lines resistant to either vemurafenib (PLX) or trametinib (TRA).

ABSTRACT: Whole-exome sequencing was performed on DNA samples extracted from seven melanoma cell lines resistant to either vemurafenib (BRAF V600E inhibitor) or trametinib (MEK1/2 inhibitor). The aim of the experiment was to search for genetic alterations responsible for phenotypic diversity of melanoma cell lines reported at the level of cell morphology, activity of signaling pathways essential for melanoma development and progression, and resistance to targeted therapeutics.

INSTRUMENT(S): Illumina HiSeq 4000

ORGANISM(S): Homo sapiens

SUBMITTER: Mariusz Hartman

PROVIDER: E-MTAB-7991 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Whole-exome sequencing of genomic DNA extracted from patient-derived melanoma cell lines resistant to vemurafenib (PLX) or trametinib (TRA)

Project description:Whole-exome sequencing was performed on DNA samples extracted from seven melanoma cell lines resistant to either vemurafenib (BRAF V600E inhibitor) or trametinib (MEK1/2 inhibitor). The aim of the experiment was to search for genetic alterations responsible for phenotypic diversity of melanoma cell lines reported at the level of cell morphology, activity of signaling pathways essential for melanoma development and progression, and resistance to targeted therapeutics.

2018-10-20 | E-MTAB-7248 | biostudies-arrayexpress

Whole-exome sequencing of genomic DNA extracted from patient-derived melanoma cell lines resistant to vemurafenib (PLX).

Project description:Whole-exome sequencing was performed on DNA sample extracted from one melanoma cell line resistant to vemurafenib (BRAF V600E inhibitor). The aim of the experiment was to search for genetic alterations responsible for phenotypic diversity of melanoma cell lines reported at the level of cell morphology, activity of signaling pathways essential for melanoma development and progression, and resistance to targeted therapeutics.

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Whole-exome sequencing of genomic DNA extracted from patient-derived melanoma cell lines grown in vitro.

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2018-07-12 | E-MTAB-6978 | 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

Insulin Reduces the Efficacy of Vemurafenib and Trametinib in Melanoma Cells.

Project description: Not available

| S-EPMC7501594 | biostudies-literature

Trametinib with or without vemurafenib in BRAF mutated non-small cell lung cancer.

Project description: Not available

| S-EPMC4338247 | biostudies-literature

Transcription profiling of human tissue samples to identify novel genes associated with malignant melanoma but not benign melanocytic lesions

Project description:A number of melanoma specific genes were identified to differentiate clinical relevant tissue samples containing benign from malignant melanocytes. Experiment Overall Design: 7 normal skin, 18 nevi and 45 melanoma samples

2007-09-06 | E-GEOD-3189 | biostudies-arrayexpress

Quantitative proteomics links the intermediate filament nestin to vemurafenib resistance in melanoma cell lines

Project description:Targeted inhibition of mutated kinases using selective MAP kinase inhibitors in malignant melanoma often results in temporary improvement of the metastatic disease followed by rapid development of resistance. To gain insights in molecular processes that govern resistance, we performed SILAC-based quantitative proteomics profiling of vemurafenib-resistant and -sensitive melanoma cells. Among downregulated proteins in vemurafenib-resistant cell lines we detected multiple proteins involved in cytoskeletal organization and signaling, including the intermediate filament nestin, which was one of the most down-regulated proteins. Previous studies showed that nestin is expressed in various types of solid tumors and its abundance correlates with malignant phenotype of transformed cells. However, the role of nestin in cancer cells with regard to acquired resistance is still poorly understood. We performed CRISPR/Cas9 knockout of the nestin gene (NES) in vemurafenib-sensitive cells and showed that loss of nestin leads to increased cellular proliferation and colony formation upon treatment with BRAF and MEK inhibitors. Moreover, nestin depletion led to increased invasiveness and metalloproteinase activity similar to resistant phenotype of melanoma cells. Finally, phosphoproteome analysis revealed that nestin depletion influenced signaling through integrin and PI3K-Akt-mTOR pathways and led to increased focal adhesion kinase expression and phosphorylation. Taken together, our results reveal that nestin is associated with acquired vemurafenib resistance in melanoma cell lines.

2019-05-14 | PXD010683 | Pride

Loss of 5-hydroxymethylcytosine is an epigenetic hallmark of melanoma

Project description:DNA methylation at the 5-position of cytosine (5-mC) is a key epigenetic mark critical for varius biological and pathological processes. 5-mC can be converted to 5-hydroxymethylcytosine (5-hmC) by the Ten-Eleven Translocation (TET) family of DNA hydroxylases. Here we report that "loss of 5-hmC" is an epigenetic hallmark of melanoma with diagonostic and prognostic implications. Genome-wide mapping of 5-hmC in nevi and melanomas for the first time revealed loss of 5-hmC landscape in the melanoma epigenome. Downregulation of Isocitrate Dehydrogenase 2 (IDH2) and TET family enzymes proved to be one of the mechanisms underlying the loss of 5-hmC during melanoma development, and rebuilding the 5-hmC landscape in the melanoma epigenome by reintroducing active TET2 or IDH2 suppressed melanoma growth and increased tumor-free survival. Thus, our study establishes that "loss of 5-hmC" is a new epigenetic hallmark of melanoma and links IDH and TET family enzymes-mediated 5-hmC putative tumor suppressor pathway to the suppression of melanoma progression. Determine the genome-wide distribution of 5mC and 5hmC in benign nevus tissue, melanoma tissue, A2058 MOCK cells (overexpressing empty vector), A2058 TET2 cells (overexpressing wild type human TET), and A2058 TET2M cells (overexpressing mutant human TET).

2012-09-18 | E-GEOD-38231 | biostudies-arrayexpress

Vemurafenib induces a noncanonical senescence-associated secretory phenotype in melanoma cells which promotes vemurafenib resistance

Project description:To explore the characteristics of senescent melanoma cells induced by vemurafenib or cisplatin, melanoma A375 cells were treated with vemurafenib and cisplatin, respectively. The senescent phenotypes were verified by β-gal staining, EdU assay, cell morphology and the senescence-related pathways. RNA-seq was performed to explore the differentially expressed genes in the senescent cells induced by vemurafenib or cisplatin.

2023-07-07 | GSE209769 | GEO

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