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WM164 BRAF mutant Melanoma cells were treated with 500nM PLX4032 for 60 days and their gene expression was compared to parent cells exposed to a corresponding concentration of DMSO.

ABSTRACT: WM164 BRAF mutant Melanoma cells were treated with 500nM PLX4032 for 60 days and their gene expression was compared to parent cells exposed to a corresponding concentration of DMSO.

PROVIDER: PRJNA561544 | ENA |

REPOSITORIES: ENA

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WM164 BRAF mutant Melanoma cells were treated with 500nM PLX4032 for 60 days and their gene expression was compared to parent cells exposed to a corresponding concentration of DMSO.

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Epigenome analysis of Control and PLX4032 Resistant Clones with EPIC array.

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Transcriptomic Analysis of Control and PLX4032 Resistant Clones with RNA Sequencing

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RNA-Seq analysis (long-reads) of human parental M238P and BRAF inhibitors-resistant M238R melanoma cells

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Gene and microRNA expression profiling of a melanoma cell line resistant to BRAF inhibitor PLX4032 compared to the parental sensitive counterpart (mRNA)

Project description:Gene and microRNA expression profiles were generated for a melanoma cell line resistant to the BRAF inhibitor PLX4032 and its parental cell line in order to identify altered gene-microRNA regulatory networks. Results showed that CCL2 acts as an autocrine factor and coordinately regulates, via HIF1, miR-34a, miR-100 and miR-125b, which are involved in cell proliferation and apoptosis. Inhibition of CCL2 and of the specific miRNAs restores sensitivity to BRAF inhibitors.

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Gene and microRNA expression profiling of a melanoma cell line resistant to BRAF inhibitor PLX4032 compared to the parental sensitive counterpart (miRNA)

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Gene expression profiling of melanoma cell lines with acquired resistance to the BRAF inhibitor PLX4032 and the parental sensitive counterparts and of melanoma cell lines intrinsically resistant.

Project description:Targeted therapy with small molecules inhibiting BRAF and MEK kinase represents a therapeutic option in advanced metastatic melanoma although drug resistance limits the achievement of persistent cures. The genomic analyses of tumors from patients developing treatment resistance indicate that drug tolerance may result from non-mutational events occurring in the tumor microenvironment. To identify tumor specific transcriptional changes related to resistance to the BRAF-inhibitor PLX4032, cell lines with acquired resistance to PLX4032 were generated from six sensitive melanoma lines by chronic in vitro drug exposure (Vergani E, Oncotarget 2016) and analyzed for gene expression profiles; in addition a set of cell lines with intrinsic resistance was included for comparison. Cell lines were obtained from metastatic surgical specimens and were previously genetically characterized (Daniotti M, Oncogene 2004; Vergani E, JID 2022, accepted).

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Parent vs. Induced drug tolerant cells Microarray Analysis

Project description:WM164 BRAF mutant Melanoma cells were treated with 500nM PLX4032 for 16 days and their gene expression was compared to parent cells kept in DMSO.

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