Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

The AP-1 transcription factor FOSL1 causes melanocyte reprogramming and transformation

ABSTRACT: The MAPK pathway is activated in the large majority of melanomas and is the subject of several therapeutic approaches. Under normal conditions, it quickly raises the so-called immediate early response, which encompasses the transient transcription of several genes belonging to the AP-1 transcription factor family. Under pathological conditions such as consistent MAPK pathway overactivation due to oncogenic alterations occurring in melanoma, these genes are permanently expressed. The consequences of a permanent expression of these genes are currently unknown.

ORGANISM(S): Homo sapiens

PROVIDER: GSE85086 | GEO | 2017/08/02

SECONDARY ACCESSION(S): PRJNA336110

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

NF1 regulates mesenchymal glioblastoma plasticity and aggressiveness through the AP-1 transcription factor FOSL1.

Project description:The molecular basis underlying glioblastoma (GBM) heterogeneity and plasticity is not fully understood. Using transcriptomic data of human patient-derived brain tumor stem cell lines (BTSCs), classified based on GBM-intrinsic signatures, we identify the AP-1 transcription factor FOSL1 as a key regulator of the mesenchymal (MES) subtype. We provide a mechanistic basis to the role of the neurofibromatosis type 1 gene (NF1), a negative regulator of the RAS/MAPK pathway, in GBM mesenchymal transformation through the modulation of FOSL1 expression. Depletion of FOSL1 in NF1-mutant human BTSCs and Kras-mutant mouse neural stem cells results in loss of the mesenchymal gene signature and reduction in stem cell properties and in vivo tumorigenic potential. Our data demonstrate that FOSL1 controls GBM plasticity and aggressiveness in response to NF1 alterations.

| S-EPMC8370767 | biostudies-literature

Fosl1/FRA1 and pancreatic cancer

Project description:AP1/Fra1 confers resistance of pancreatic cancer cells to inhibitors of the MAPK cascade

| PRJEB52257 | ENA

RNA-seq of Glioma Neural Stem (GNS) cell line G144 after MEK inhibition in wild type (WT) and CIC (Capicua) depleted cells.

Project description:We identified genome-wide binding patterns of CIC in several different cell types and find that CIC target genes are enriched for MAPK effector genes involved in cell cycle regulation and proliferation. CIC binding to its target genes is abolished by high MAPK activity, which leads to hyperacetylation and their transcriptional activation. Inhibition of MAPK signaling via MEK inhibition leads to recruitment of CIC to its target genes. ChIP-seq data of G144 cells after MEK inhibition and CIC knockout is available under accession E-MTAB-6682

2018-05-31 | E-MTAB-6681 | biostudies-arrayexpress

ChIP-seq of CIC (Capicua) and histone marks (H3K9ac, H3K27ac and H3K4me1) in glioma neural stem cells (GNS) G144, human foetal neural stem cells (hNSC) and mouse embryonic stem cells (mESC),

Project description:We identified genome-wide binding patterns of CIC in several different cell types and find that CIC target genes are enriched for MAPK effector genes involved in cell cycle regulation and proliferation. CIC binding to its target genes is abolished by high MAPK activity, which leads to hyperacetylation and their transcriptional activation. Inhibition of MAPK signaling via MEK inhibition leads to recruitment of CIC to its target genes. Expression data of G144 cells after MEK inhibition and CIC knockout is available under accession E-MTAB-6681

2018-05-31 | E-MTAB-6682 | biostudies-arrayexpress

Dual-omics reveals the different roles of α1 and β-adrenergic receptors in acute sympathetic stress-induced cardiac inflammation

Project description:Sympathetic overactivation under strong acute stresses triggers acute cardiovascular events including myocardial infarction (MI), sudden cardiac death, and stress cardiomyopathy. α1-ARs and β-ARs, two dominant subtypes of adrenergic receptors in the heart, play a significant role in the physiological and pathologic regulation of these processes. However, little is known about the functional similarities and differences between α1- and β-ARs activated temporal responses in stress-induced cardiac pathology. In this work, we systematically compared the cardiac temporal genome-wide profiles of acute α1-AR and β-AR activation in the mice model by integrating transcriptome and proteome. We found that α1- and β-AR activations induced sustained and transient inflammatory gene expression, respectively. Particularly, the overactivation of α1-AR but not β-AR led to neutrophil infiltration at 1 day, which was closely associated with the up-regulation of chemokines, activation of NF-κB pathway, and sustained inflammatory response. Furthermore, there are more metabolic disorders under α1-AR overactivation compared with β-AR overactivation. These findings provide a new therapeutic strategy that besides using β-blocker as soon as possible, blocking α1-AR within one day should also be considered in the treatment of acute stress associated cardiovascular diseases.

2023-01-19 | PXD036011 | Pride

Dual-omics reveals the different roles of α1 and β-adrenergic receptors in acute sympathetic stress-induced cardiac inflammation

2023-01-13 | GSE211134 | GEO

Proteomics of WT and bleached Euglena

Project description:In this study, the whole-genome proteome with dark-adapted E. gracilis strain (WT) and permanently ofloxacin-bleached mutant (B2) was compared under the light exposure after 0 h, 12 h, and 72h.

2022-04-04 | PXD030414 | Pride

Trophoblast giant cell underrepresentation

Project description:This SuperSeries is composed of the SubSeries listed below. The BioProject ID on this superSeries record also encompasses a genome sequencing project under BioProject PRJNA213010.

2014-05-29 | GSE50585 | GEO

Recurrent FOSL1 rearrangements in desmoplastic fibroblastoma.

Project description:The FOS gene family has been implicated in tumourigenesis across several tumour types, particularly mesenchymal tumours. The rare fibrous tumour desmoplastic fibroblastoma is characterised by overexpression of FOSL1. However, previous studies using cytogenetic and molecular techniques did not identify an underlying somatic change involving the FOSL1 gene to explain this finding. Prompted by an unusual index case, we report the discovery of a novel FOSL1 rearrangement in desmoplastic fibroblastoma using whole-genome and targeted RNA sequencing. We investigated 15 desmoplastic fibroblastomas and 15 fibromas of tendon sheath using immunohistochemistry, in situ hybridisation and targeted RNA sequencing. Rearrangements in FOSL1 and FOS were identified in 10/15 and 2/15 desmoplastic fibroblastomas respectively, which mirrors the pattern of FOS rearrangements observed in benign bone and vascular tumours. Fibroma of tendon sheath, which shares histological features with desmoplastic fibroblastoma, harboured USP6 rearrangements in 9/15 cases and did not demonstrate rearrangements in any of the four FOS genes. The overall concordance between FOSL1 immunohistochemistry and RNA sequencing results was 90%. These findings illustrate that FOSL1 and FOS rearrangements are a recurrent event in desmoplastic fibroblastoma, establishing this finding as a useful diagnostic adjunct and expanding the spectrum of tumours driven by FOS gene family alterations. © 2022 The Authors. The Journal of Pathology published by John Wiley & Sons Ltd on behalf of The Pathological Society of Great Britain and Ireland.

| S-EPMC10107450 | biostudies-literature

Trophoblast giant cell underrepresentation

2014-05-29 | E-GEOD-50585 | biostudies-arrayexpress