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Molecular mechanisms of BCAT1 in ASK120067-resistant NSCLC cells

ABSTRACT: To investigate the mechanism of BCAT1 in mediating resistance to third-generation EGFR-TKI, we employed RNA-seq analysis to compare the transcriptome signature of ASK120067-resistant NSCLC cells with or without BCAT1 knockdown. Here, gene set enrichment (GSEA) revealed a significant decrease in the expression of genes in glycolysis pathway following small interfering RNA (siRNA)-mediated BCAT1 knockdown, which indicated the role for BCAT1 in supporting TKI resistance through upregulation of glycolysis.

ORGANISM(S): Homo sapiens

PROVIDER: GSE247584 | GEO | 2024/08/15

REPOSITORIES: GEO

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BCAT1 contributes to the developmentproliferation and leukemogenesis of TKI-resistant CML

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BCAT1 Confers Resistance to EGFR TKIs through α-KG-dependent Epigenetic Regulation of the Glycolysis Pathway in NSCLC

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Molecular mechanisms of BCAT1 in ASK120067-resistant NSCLC cells

Project description:Molecular mechanisms of BCAT1 in ASK120067-resistant NSCLC cells

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Project description:About 10% of all NSCLC patients respond to gefitnib treatment and all of these patients will acquire resistance to the EGFR TKI. We used microarray to look at global gene expression changes in untreated cells vs gefitinib treated cells to identify key characters for the acquisition of resistance. NSCLC cells, H322c, were cultured 4 days in media containing 1?M gefitinib or 0.1% DMSO as a control. On day 4, RNA was extracted and submitted for microarray hybridization.

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2016-07-01 | E-GEOD-75307 | biostudies-arrayexpress

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