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E-MTAB-6483

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

PROVIDER: E-MTAB-6483 | ExpressionAtlas | 2025-01-23

REPOSITORIES: ExpressionAtlas

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			Action	DRS
	E-MTAB-6483-analysis-methods.tsv	Tabular
	E-MTAB-6483-analytics.tsv	Tabular
	E-MTAB-6483-atlasExperimentSummary.Rdata	Rdata
	E-MTAB-6483-configuration.xml	Xml
	E-MTAB-6483-g2_g1-mvaPlot.png	Other

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

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

| PRJEB24899 | ENA

RNA-seq to investigate impact of treatment of KRAS mutant A549 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-6483 | biostudies-arrayexpress

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

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

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

2018-06-01 | E-MTAB-6485 | biostudies-arrayexpress

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

| PRJEB24900 | ENA

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

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

| PRJEB24901 | ENA

E-MTAB-6485

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

2025-01-23 | E-MTAB-6485 | ExpressionAtlas

E-MTAB-6486

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

2025-01-23 | E-MTAB-6486 | ExpressionAtlas

KDM1A confers invasive and metastatic attributes in lung adenocarcinoma by modulating a non-canonical Integrin ß3-KRAS signaling pathway

Project description:KRAS mutations occur in approximately 25% of non-small cell lung cancer (NSCLC). They account for the therapy resistance to EGFR inhibitors and are suggested to be difficult to target by specific drugs. Therefore, new therapies for KRAS mutant NSCLC are urgently needed. The histone H3K4 and H3K9 di/mono-demethylase KDM1A is a key epigenetic writer, aberrantly upregulated in many cancer types, including NSCLC. In order to understand the functional role of KDM1A in the progression of lung adenocarcinoma, KDM1A expression profiles were analysed in tissue microarrays (TMAs) including 182 lung adenocarcinoma. KDM1A expression correlated with high grade and metastasized tumor. To investigate the impact of KDM1A in lung adenocarcinoma development, we used the KRAS mutated A549 cell line to establish a shRNA-mediated stable KDM1A knockdown cell clone. Unexpectedly, KDM1A knockdown had only a slight effect on retardation of cell growth. However, cell invasion and self-renewal capability was significantly decreased by KDM1A inhibition. KDM1A knockdown in A549 cell resulted in a dramatic change in the transcriptome profile as determined by RNA-Seq. Interestingly, genes involved in the KRAS signature and lung epithelial marker genes were significantly affected upon KDM1A knockdown. Ingenuity pathway analysis also suggested that the alternative integrin β3-KRAS signaling axis, which is involved in stem cell like properties, is abrogated upon KDM1A knockdown. Indeed, Integrin β3 and its non-canonical ligand galectin-3 were strongly downregulated and their downstream NF-κB activity was decreased upon KDM1A knockdown. Finally, correlation of KDM1A to the Integrin β3 level was validated in TMAs.

2017-03-13 | GSE86874 | GEO

Sotorasib Resistance in KRAS G12C-Mutant Invasive Mucinous Adenocarcinoma with Implications for VEGF-A

Project description:Invasive mucinous adenocarcinoma (IMA) is a rare subtype of lung adenocarcinoma with a poor prognosis. Compared to non-small cell lung cancer (NSCLCs), IMA more frequently harbors KRAS mutations in the order KRAS p.G12V, p.G12D, and p.G12C. This report describes a patient with KRAS p.G12C-mutant IMA treated with sotorasib. To date, no studies have investigated the therapeutic efficacy or resistance mechanisms of sotorasib in IMA. The patient was treated with carboplatin and pemetrexed, followed by sotorasib upon disease progression. While the primary lung lesions responded well, metastatic thoracic lymph node lesions continued to increase. A pathological autopsy was performed with the family’s consent to investigate potential resistance mechanisms. RNA sequencing and additional analyses revealed increased VEGF-A expression in metastatic lymph node lesions, suggesting a role in sotorasib resistance. These findings provide insights into the molecular mechanisms underlying treatment resistance in KRAS p.G12C-mutant IMA.

2025-05-02 | GSE295712 | GEO

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