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RNA-seq to investigate impact of treatment of KRAS mutant NCI-H2009 lung adenocarcinoma cells with the multi-ERBB inhibitor Neratinib

ABSTRACT: RNA-seq to investigate impact of treatment of KRAS mutant NCI-H2009 lung adenocarcinoma cells with the multi-ERBB inhibitor Neratinib

PROVIDER: PRJEB24901 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR2287664_1.fastq.gz	Fastqsanger.gz
	ERR2287664_2.fastq.gz	Fastqsanger.gz
	ERR2287665_1.fastq.gz	Fastqsanger.gz
	ERR2287665_2.fastq.gz	Fastqsanger.gz
	ERR2287666_1.fastq.gz	Fastqsanger.gz

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RNA-seq to investigate impact of treatment of KRAS mutant NCI-H2009 lung adenocarcinoma cells with the multi-ERBB inhibitor Neratinib

Project description:KRAS mutation is widely presumed to confer independence from upstream RTK signalling, however emerging evidence from mouse models of lung cancer suggests that ERBB RTKs may amplify signalling through RAS isoforms and participate in mutant RAS-driven lung cancer. This is one of 3 datasets where we examined the transcriptional impact of treatment of KRAS mutant human lung cancer cell lines with the multi-ERBB inhibitor Neratinib

2018-06-01 | E-MTAB-6486 | biostudies-arrayexpress

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RNA-seq to investigate impact of treatment of KRAS mutant NCI-H358 lung adenocarcinoma cells with the multi-ERBB inhibitor Neratinib

Project description:RNA-seq to investigate impact of treatment of KRAS mutant NCI-H358 lung adenocarcinoma cells with the multi-ERBB inhibitor Neratinib

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RNA-seq to investigate impact of treatment of KRAS mutant A549 lung adenocarcinoma cells with the multi-ERBB inhibitor Neratinib

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¬The EGFR/ErbB inhibitor neratinib promotes apoptosis and clearance by airway macrophages

Project description:Dysregulated neutrophilic inflammation can be highly destructive in chronic inflammatory diseases due to prolonged neutrophil lifespan and continual release of histotoxic mediators in inflamed tissues. Inducing neutrophil apoptosis, an immunologically silent form of cell death, may be beneficial in these diseases, provided that the apoptotic neutrophils are efficiently cleared from the tissue. Our previous research identified ErbB inhibitors as able to induce neutrophil apoptosis and reduce neutrophilic inflammation both in vitro and in vivo (Rahman et al. 2019). Here we expand on that work using a clinical ErbB inhibitor, neratinib, which has the potential to be repurposed in inflammatory diseases. We show that neratinib reduces neutrophilic migration to an inflammatory site in zebrafish larvae. Neratinib upregulates efferocytosis and reduces the number of dead neutrophils in mouse models of acute, but not chronic, lung injury, suggesting the drug may have therapeutic benefits in acute inflammatory settings. Phosphoproteomics analysis of human neutrophils shows that neratinib modifies the phosphorylation of proteins regulating apoptosis, migration and efferocytosis. This work identifies a potential efficacious mechanism for neratinib in acute lung inflammation by upregulating the clearance of dead neutrophils, and examination of the neutrophil phosphoproteome gives insight into the mechanisms by which this may be occurring.

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Identification of cells exhibiting elevated ERBB network activity in KRas/ Myc-driven lung tumours

Project description:Our lab has identified a completely unexpected requirement for ERBB signalling in KRAS‐driven Lung Adenocarcinoma (LuAd). We have shown that this requirement is present from the very outset of lung tumour initiation, and, crucially, we have found a pronounced increase in ERBB signalling during progression from low grade adenocarcinoma to locally invasive disease. We hypothesize that this increased activity, which manifests as strongly elevated expression of multiple EGF/ERBB-family ligands, such as Amphiregulin (AREG), and paracrine activation of ERBB2 on infiltrating macrophages, may be exploited for early detection of KRAS‐ driven malignancy. Alongside a more general increase in AREG expression as tumours progress to higher grade disease, we find individual cells that express extremely high levels of AREG mRNA. We refer to these cells as AREG super-expressers and their lineage identity is unknown. Cell morphology suggests they maybe epithelial, however, unlike the bulk of tumours, these cells fail to express the lung epithelial marker SPC and staining for cytokeratins is inconclusive. Their detection at and adjacent to the tumour:normal interface suggests that they maybe disseminating tumour cells undergoing EMT. Alternatively, they may belong to another lung-resident or infiltrating population, induced to express AREG through direct contact with tumour cells. Immediately adjacent to progressing tumours we find large numbers of F4/80-positive macrophages that stain strongly for tyrosine phosphorylated ERBB2 (p-Tyr-ERBB2), suggesting paracrine activation in response to local production of ERBB ligands. The aim of this part of the work is to identify the cell lineage of the AREG superexpressers and to investigate the effect of ERBB-inhibition using the multi-ERBB inhibitor Neratinib.

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