Table 3.

Table of all the preclinical studies evidencing the role of MET in chemoresistance and the mechanisms involved.

Cell lines in blue font: paired isogenic chemosensitive and chemoresistant cell lines. (Note - some cell lines placed in the chemosensitive category in this table have also been used as a model to study chemoresistance as their chemosensitivity may be reduced). Red box: MET overexpressed in chemoresistant cell line compared to parental cells. Yellow box: constitutive activation of MET. Orange box: MET overexpressed and constitutively active. Green dot: HGF expressed. The darker or lighter green indicate an increase or a decrease of HGF in chemoresistant cells versus chemosensitive cells.

MET-stimulated cellular functions which promote chemoresistance: A: apoptosis inhibition, R: DNA repair enhancement, CC: cell cycle progression, D: drug efflux, P: increased proliferation, E: increased EMT, S: enhanced cancer stem cells survival and proliferation, AE: altered endothelial cell behaviour, H: increased intra-tumoural hypoxia.

NSCLC non-small cell lung cancer, SCLC small cell lung cancer, PDAC pancreatic ductal adenocarcinoma, HCC hepatocellular carcinoma.