c-Met signaling in the development of tumorigenesis and chemoresistance: Potential applications in pancreatic cancer

Table 2 Mechanisms of hepatocyte growth factor-mesenchymal-epithelial transition factor induced chemoresistance in different cancer types

Cancer type	Chemotherapy	Mechanism of HGF-MET signaling in chemoresistance
Multiple myeloma	Bortezomib	MET overexpression: Apoptotic resistance via PI3K-Akt activation[92]
Glioblastoma	Radiation, cisplatin, camptothecin, adriamycin, and taxol groups	Addition of HGF: Anti-apoptotic effects via PI3K-Akt dependent pathways[91]
Rhabdomyosarcoma	Vincristine/etoposide, radiation	Addition of HGF: Enhanced migration, MMP secretion, PI3K-Akt activation[119]
Non-small cell lung carcinoma	Cisplatin	Addition of HGF: Downregulation of apoptosis-inducing factor (AIF)[87]
Non-small cell lung carcinoma	Erlotinib	c-met amplification: Activation of EGFR, preservation of PI3K-Akt activation[88]
Gastric adenocarcinoma	Adriamycin	Addition of HGF: Anti-apoptotic effects via PI3K-Akt upregulation[93]
Pancreatic adenocarcinoma	Gemcitabine	MET overexpression: Anti-apoptotic effects via PI3K-Akt activation, induction of EMT-like changes[94,95]
Ovarian adenocarcinoma	Carboplatin/paclitaxel	MET overexpression: Apoptotic resistance via PI3K-Akt activation[89,90]

MET: Mesenchymal-epithelial transition factor; PI3K: Phosphoinositide 3-kinase; Akt: Protein kinase B; HGF: Hepatocyte growth factor; MMP: Matrix metalloproteinase; EGFR: Epidermal growth factor receptor; EMT: Epithelial-mesenchymal transition.