Epithelial-to-mesenchymal transition defines feedback activation of receptor tyrosine kinase signaling induced by MEK inhibition in KRAS mutant lung cancer. Homo sapiens

To determine the difference of gene expression profile in epithelial and mesenchymal KRAS mutant lung cancers, epithelial NCI-H358 cells were treated with TGFβ1 (4 ng/mL) or PBS for 14 days in order to induce epithelial to mesenchymal transition (EMT). Gene expression was determined in NCI-H358 cells before and after EMT induction. In addition, in order to investigate the effect of a MEK inhibitor trametinib on gene expression, mesenchymal NCI-H1792 cells were treated with 50 nM trametinib for 48 hours. Gene expression of H1792 cells for pre- and post-trametinib treatement was determined. Overall design: H358 was induced EMT by treated with TGF-beta. H1792 were treated with trametinib for 48 hours. Two independent experiments were performed