As an upstream signaling pathway involved in the regulation of the cell cycle and apoptosis in colon cancer, the impact of compound 1t on the MET/PI3K/AKT/mTOR intracellular pathway was assessed which revealed that MET receptor tyrosine kinase and its downstreams were inhibited in a concentration-dependent manner, suggesting that MET receptor tyrosine kinase is the molecular target mediating the antiproliferative activity of compound 1t in HCT116 colon cancer cells. This evidence concerns the gene MET and colonic neoplasm.