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World J Gastroenterol. Jul 14, 2014; 20(26): 8458-8470
Published online Jul 14, 2014. doi: 10.3748/wjg.v20.i26.8458
c-Met signaling in the development of tumorigenesis and chemoresistance: Potential applications in pancreatic cancer
Daniel Delitto, Eva Vertes-George, Steven J Hughes, Kevin E Behrns, Jose G Trevino
Daniel Delitto, Steven J Hughes, Kevin E Behrns, Jose G Trevino, Department of Surgery, University of Florida-Gainesville, Gainesville, FL 32610, United States
Eva Vertes-George, Department of Pathology, University of Florida-Gainesville, Gainesville, FL 32610, United States
Author contributions: All the authors contributed to this manuscript.
Correspondence to: Jose G Trevino, MD, Department of Surgery, University of Florida-Gainesville, 1600 SW Archer Rd, Rm 6175, PO Box 100109, Gainesville, FL 32610, United States. jose.trevino@surgery.ufl.edu
Telephone: +1-352-2737967 Fax: +1-352-2650761
Received: September 23, 2013
Revised: December 18, 2013
Accepted: April 1, 2014
Published online: July 14, 2014
Processing time: 294 Days and 7.8 Hours
Abstract

Pancreatic ductal adenocarcinoma is the 4th leading cause of cancer deaths in the United States. The majority of patients are candidates only for palliative chemotherapy, which has proven largely ineffective in halting tumor progression. One proposed mechanism of chemoresistance involves signaling via the mesenchymal-epithelial transition factor protein (MET), a previously established pathway critical to cell proliferation and migration. Here, we review the literature to characterize the role of MET in the development of tumorigenesis, metastasis and chemoresistance, highlighting the potential of MET as a therapeutic target in pancreatic cancer. In this review, we characterize the role of c-Met in the development of tumorigenesis, metastasis and chemoresistance, highlighting the potential of c-Met as a therapeutic target in pancreatic cancer.

Keywords: Pancreatic adenocarcinoma; c-Met; Chemoresistance; Receptor tyrosine kinase

Core tip: As one of the leading causes of cancer-related deaths, pancreatic cancer remains elusive to our current therapeutic options. These modest advances in current therapies for pancreatic cancer have led to the recognition and development of targeted therapies toward tyrosine kinase receptors such as the c-Met receptor. In this review, we characterize the role of c-Met in the development of tumorigenesis, metastasis and chemoresistance, highlighting the potential of c-Met as a therapeutic target in pancreatic cancer.