MET Amplified Gastric Cancer Cell Lines +/- Crizotinib

ABSTRACT: MET amplification is present in 20% of gastric cancers and has been confirmed as a therapeutic target in clinical trials. The molecular mechanisms of response and resistance to MET inhibitors are not well understood. We investigated the determinants of MET dependency in human gastric cancer. MET inhibition inhibited proliferation and induced cell death only in MET-amplified gastric cancer cell lines. The effects on growth arrest were stronger than the effects on cell death. To identify possible resistance mechanisms, we performed whole-genome mRNA expression profiling. Molecular changes related to autophagy were among the top alterations observed. Consistent with these findings, autophagy levels increased in a concentration-dependent manner when MET-amplified cells were exposed to crizot

ORGANISM(S): Homo sapiens

SUBMITTER: Rebecca Schroeder 

PROVIDER: E-GEOD-77320 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress