Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

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

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE68839 | GEO | 2016/02/01

SECONDARY ACCESSION(S): PRJNA283887

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

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

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

Project description:Genome wide DNA methylation profiling of control and PLX4032 resistant clones to identify resistance-associated methylome alternations, and to integrate with transcriptome analysis. Results provide insight into clonal epigentic adaption of PLX4032 resistance in BRAF V600E melanoma.

2020-09-20 | GSE137452 | GEO

Transcriptomic Analysis of Control and PLX4032 Resistant Clones with RNA Sequencing

Project description:NGS-derived transcriptome profiling (RNA-seq) of control and PLX4032 resistant clones to identify resistance-associated gene-expression changes and pathway enrichments, and to integrate with exome and methylome analysis. Results provide insight into PLX4032 resistance in BRAF V600E melanoma.

2020-09-20 | GSE137309 | GEO

COLO829 treatment with PLX4032 and/or MITF knockdown

Project description:Thousands of enhancers are characterized in the human genome, yet few have been shown important in cancer. Inhibiting oncokinases, such as EGFR, ALK, HER2, and BRAF, is a mainstay of current cancer therapy but is hindered by innate drug resistance mediated by upregulation of the HGF receptor, MET. The mechanisms mediating such genomic responses to targeted therapy are unknown. Here, we identify lineage-specific MET enhancers for multiple common tumor types, including a melanoma lineage-specific MET enhancer that displays inducible chromatin looping and MET gene induction upon BRAF inhibition. Epigenomic analysis demonstrated that the melanocyte-specific transcription factor, MITF, mediates this enhancer function. Targeted genomic deletion (<7bp) of the MITF motif within the MET enhancer suppressed inducible chromatin looping and innate drug resistance, while maintaining MITF-dependent, inhibitor-induced melanoma cell differentiation. Epigenomic analysis can thus guide functional disruption of regulatory DNA to decouple pro- and anti-oncogenic functions of tumor lineage-enriched transcription factors mediating innate resistance to oncokinase therapy. COLO829 human melanoma cell line harboring the BRAFV600E mutation was treated with BRAF inhibtior PLX4032 (Vemurafenib) and/or a hairpin against MITF

2014-01-14 | E-GEOD-50649 | biostudies-arrayexpress

microRNA-seq reveals microRNAs under the regulation of miR-125b in NCCIT tumor cells

Project description:To investigate the role and mechanism of miR-125b on NCCIT cells without bias, we analyzed differentially expression microRNA profile among miR-125b antagomir-, miR-125b agomir-, and negative control-transfected NCCIT tumor cells by microRNA-seq.

2018-11-30 | GSE123156 | GEO

The Transcriptome of PLX4032 resistance

Project description:We have collected material from a patient who had BrafV600E mutant melanoma that was treated with PLX4032. We have germline DNA from the patient and DNA and RNA from distinct lesions before and after treatment with PLX4032. We have transcriptome sequenced these samples to obtain a snap shot of the mechanisms of resistance that are operative.

2013-06-07 | E-ERAD-138 | biostudies-arrayexpress

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

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

Safety Study of PLX4032 in Patients With Solid Tumors

Project description:The primary objective of this FIH study is to assess the safety and pharmacokinetics of PLX4032 in patients with solid tumors. The secondary objective is to assess the pharmacodynamic activity in paired biopsy specimens obtained from patients with malignant melanoma who have the V600E BRAF oncogenic mutation.

| 2034890 | ecrin-mdr-crc

Identification of SART3 as a pre-miR-34a–binding protein

Project description:MicroRNAs (miRNAs or miRs) are small, noncoding RNAs that are implicated in the regulation of nearly all biological processes. Global miRNA biogenesis is altered in many cancers and RNA-binding proteins (RBPs) have been shown to play a role in this process, presenting a promising avenue for targeting miRNA dysregulation in disease. miR-34a exhibits tumor-suppressive functions by targeting cell cycle regulators CDK4/6 and anti-apoptotic factor Bcl-2, among other regulatory pathways such as Wnt, TGF-, and Notch signaling. Many cancers show downregulation or loss of miR-34a, and synthetic miR-34a supplementation has been shown to inhibit tumor growth in vivo; however, the post-transcriptional mechanisms by which miR-34a is lost in cancer are not entirely understood. Here, we have used a proteomics-mediated approach to identify Squamous cell carcinoma antigen recognized by T-cells 3 (SART3) as a putative pre-miR-34a-binding protein. SART3 is a spliceosome recycling factor and nuclear RBP with no previously reported role in miRNA regulation. We demonstrate that SART3 binds pre-miR-34a with specificity over pre-let-7d and begin to elucidate a new functional role for this protein in non-small lung cancer cells. Overexpression of SART3 led to increased miR-34a levels, downregulation of the miR-34a target genes CDK4 and CDK6, and cell cycle arrest in the G1 phase. In vitro binding studies showed that the RNA-recognition motifs within the SART3 sequence are responsible for selective pre-miR-34a binding. Collectively, our results present evidence for an influential role of SART3 in miR-34a biogenesis and cell cycle progression.

2019-10-14 | PXD015278 | Pride

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