MET amplification, expression, and splice mutations at exon 14 result in dysregulation of the MET signaling pathway. The aim of this study was to identify the relationship between MET amplification,
protein or
mRNA expression, and mutations in
colorectal cancer (CRC). MET immunohistochemistry was used for MET
protein expression analysis, and fluorescence in situ hybridization was used for MET amplification detection. Both analyses were performed in tissue microarrays containing 294 colorectal
adenocarcinoma tissue samples and 131 samples of adjacent normal epithelial tissue. MET
mRNA expression was examined by real-time quantitative polymerase chain reaction in 72 fresh colorectal
adenocarcinoma tissue samples and adjacent normal colon tissue. Polymerase chain reaction sequencing was performed to screen for MET exon 14 splice mutations in 59 fresh CRC tissue samples. Our results showed that MET
protein expression was higher in
colorectal tumor tissue than in adjacent normal intestinal epithelium. Positive MET
protein expression was associated with significantly poorer overall survival and disease-free survival. Multivariate analysis revealed that positive MET
protein expression was an independent risk factor for disease-free survival but not for overall survival. MET
mRNA expression was upregulated in
tumor tissues compared with the adjacent normal tissues. The incidence of MET amplification was 4.4%. None of the patients was positive for MET mutation. Collectively, MET was overexpressed in colorectal
adenocarcinoma, and its positive
protein expression predicted a poorer outcome in CRC patients. Furthermore, according to our results, MET amplification and exon 14 mutation are extremely rare events in colorectal
adenocarcinoma.