Sohn SH, et al. - Researchers used human gastric cancer (GC) cell lines to characterize mesenchymal-to-epithelial transition (MET) and CD44 expression and signaling in these cell lines, and they assessed variations in the susceptibility of these lines to foretinib. They found dose-dependent inhibition of growth in c-MET-amplified MKN45 and SNU620 cells with concomitant apoptosis was induced by foretinib treatment, but these effects were not seen in c-MET-reduced MKN28 and AGS cells. In MKN45 and SNU620 cells, phosphor-c-MET, phosphor-AKT, beta-catenin, and COX-2 protein expression was significantly decreased by foretinib treatment. A significant decrease in CD44, CD44v9 (CD44 variant 9), COX-2, OCT3/4, CCND1, c-MYC, VEGFA, and HIF-1a gene expression in CD44 and MET coactivated MKN45 cells and an increase in CD44s gene expression was brought about by foretinib; in contrast, these drugs were only slightly active against SNU620 cells. As per the findings, foretinib could serve as a curative agent for the prevention or management of GCs positive for CD44v9 and c-MET.