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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

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE68841 | GEO | 2016/02/01

SECONDARY ACCESSION(S): PRJNA283867

REPOSITORIES: GEO

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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.

2016-02-01 | GSE68840 | GEO

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

2016-02-01 | GSE68839 | GEO

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

Project description:Gene and microRNA expression profiling of a melanoma cell line resistant to BRAF inhibitor PLX4032 compared to the parental sensitive counterpart

| PRJNA283867 | ENA

microRNA expression profiling of melanoma cell lines with acquired resistance to the BRAF inhibitor PLX4032 compared to the parental sensitive counterparts

Project description:microRNA expression profiles show altered patterns in cell lines with acquired resistance to the BRAF inhibitor compared to the parental cell lines, and common miRNAs regulated in the resistant variants

2020-10-02 | GSE141314 | GEO

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).

2022-06-17 | GSE201913 | GEO

The BRAF(V600E) inhibitor, PLX4032, increases type I collagen synthesis in melanoma cells.

Project description:Vertical growth phase (VGP) melanoma is frequently metastatic, a process mediated by changes in gene expression, which are directed by signal transduction pathways in the tumor cells. A prominent signaling pathway is the Ras-Raf-Mek-Erk MAPK pathway, which increases expression of genes that promote melanoma progression. Many melanomas harbor a mutation in this pathway, BRAF(V600E), which constitutively activates MAPK signaling and expression of downstream target genes that facilitate tumor progression. In BRAF(V600E) melanoma, the small molecule inhibitor, vemurafenib (PLX4032), has revolutionized therapy for melanoma by inducing rapid tumor regression. This compound down-regulates the expression of many genes. However, in this study, we document that blocking the Ras-Raf-Mek-Erk MAPK pathway, either with an ERK (PLX4032) or a MEK (U1026) signaling inhibitor, in BRAF(V600E) human and murine melanoma cell lines increases collagen synthesis in vitro and collagen deposition in vivo. Since TGFß signaling is a major mediator of collagen synthesis, we examined whether blocking TGFß signaling with a small molecule inhibitor would block this increase in collagen. However, there was minimal reduction in collagen synthesis in response to blocking TGFß signaling, suggesting additional mechanism(s), which may include activation of the p38 MAPK pathway. Presently, it is unclear whether this increased collagen synthesis and deposition in melanomas represent a therapeutic benefit or an unwanted "off target" effect of inhibiting the Ras-Raf-Erk-Mek pathway.

| S-EPMC5048745 | biostudies-literature

PLX4032, a selective BRAF(V600E) kinase inhibitor, activates the ERK pathway and enhances cell migration and proliferation of BRAF melanoma cells.

Project description:BRAF(V600E/K) is a frequent mutationally active tumor-specific kinase in melanomas that is currently targeted for therapy by the specific inhibitor PLX4032. Our studies with melanoma tumor cells that are BRAF(V600E/K) and BRAF(WT) showed that, paradoxically, while PLX4032 inhibited ERK1/2 in the highly sensitive BRAF(V600E/K), it activated the pathway in the resistant BRAF(WT) cells, via RAF1 activation, regardless of the status of mutations in NRAS or PTEN. The persistently active ERK1/2 triggered downstream effectors in BRAF(WT) melanoma cells and induced changes in the expression of a wide-spectrum of genes associated with cell cycle control. Furthermore, PLX4032 increased the rate of proliferation of growth factor-dependent NRAS Q61L mutant primary melanoma cells, reduced cell adherence and increased mobility of cells from advanced lesions. The results suggest that the drug can confer an advantage to BRAF(WT) primary and metastatic tumor cells in vivo and provide markers for monitoring clinical responses.

| S-EPMC2848976 | biostudies-literature

Gene Expression Signature of BRAF Inhibitor Resistant Melanoma Spheroids.

Project description:In vitro cell cultures are frequently used to define the molecular background of drug resistance. The majority of currently available data have been obtained from 2D in vitro cultures, however, 3D cell culture systems (spheroids) are more likely to behave similarly to in vivo conditions. Our major aim was to compare the gene expression signature of 2D and 3D cultured BRAFV600E mutant melanoma cell lines. We successfully developed BRAF-drug resistant cell lines from paired primary/metastatic melanoma cell lines in both 2D and 3D in vitro cultures. Using Affymetrix Human Gene 1.0 ST arrays, we determined the gene expression pattern of all cell lines. Our analysis revealed 1049 genes (562 upregulated and 487 downregulated) that were differentially expressed between drug-sensitive cells grown under different cell cultures. Pathway analysis showed that the differently expressed genes were mainly associated with the cell cycle, p53, and other cancer-related pathways. The number of upregulated genes (72 genes) was remarkably fewer when comparing the resistant adherent cells to cells that grow in 3D, and were associated with cell adhesion molecules and IGF1R signalling. Only 1% of the upregulated and 5.6% of the downregulated genes were commonly altered between the sensitive and the resistant spheroids. Interestingly, we found several genes (BNIP3, RING1 and ABHD4) with inverse expression signature between sensitive and resistant spheroids, which are involved in anoikis resistance and cell cycle regulation. In summary, our study highlights gene expression alterations that might help to understand the development of acquired resistance in melanoma cells in tumour tissue.

| S-EPMC7471197 | biostudies-literature

microRNA expression profiling of melanoma cell lines with acquired resistance to the BRAF inhibitor PLX4032 compared to the parental sensitive counterparts

Project description:microRNA expression profiling of melanoma cell lines with acquired resistance to the BRAF inhibitor PLX4032 compared to the parental sensitive counterparts

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Expression data of BRAF inhibitor resistant melanoma cells

Project description:We generated four drug-resistant melanoma cell lines from paired primary/metastatic cell lines using PLX4720 and used for Affymetrix Human Gene 1.0 ST array

2019-01-31 | GSE114443 | GEO

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