PT - JOURNAL ARTICLE AU - EIJI KUNII AU - HIROAKI OZASA AU - TETSUYA OGURI AU - KEN MAENO AU - SATOSHI FUKUDA AU - TAKEHIRO UEMURA AU - OSAMU TAKAKUWA AU - HIROTSUGU OHKUBO AU - MASAYA TAKEMURA AU - AKIO NIIMI TI - Reversal of c-MET-mediated Resistance to Cytotoxic Anticancer Drugs by a Novel c-MET Inhibitor TAS-115 DP - 2015 Oct 01 TA - Anticancer Research PG - 5241--5247 VI - 35 IP - 10 4099 - http://ar.iiarjournals.org/content/35/10/5241.short 4100 - http://ar.iiarjournals.org/content/35/10/5241.full SO - Anticancer Res2015 Oct 01; 35 AB - Background: The cellular N-methyl-N’-nitroso-guanidine human osteosarcoma transforming gene (c-MET) protein is the receptor tyrosine kinase for hepatocyte growth factor. We recently found that c-MET protein expression and activation were enhanced in the majority of small cell lung cancer cell lines with cytotoxic anticancer drug resistance, and that down-regulation of c-MET reduced resistance to these drugs. Materials and Methods: Expression of c-MET was studied in three non-small cell lung cancer (NSCLC) cell lines, including six resistant cell strains to cytotoxic anticancer drugs. To assess the effect of c-MET activation on drug resistance, we studied drug sensitivity in the presence of a novel c-MET inhibitor TAS-115. Results: c-MET expression and activation are also enhanced in some cytotoxic anticancer drug-resistant NSCLC cell lines, and inhibition of c-MET activation by TAS-115 reduced resistance of these cell lines to anticancer drugs. Conclusion: The mechanism of cellular resistance to anticancer drugs via hepatocyte growth factor/c-MET signal activation is not restricted to small cell lung cancer cell lines, and TAS-115 might be able to reverse the drug resistance of these cancer cells.