Field Of Vision
Copyright ©2012 Baishideng Publishing Group Co., Limited. All rights reserved.
World J Gastroenterol. Oct 14, 2012; 18(38): 5321-5323
Published online Oct 14, 2012. doi: 10.3748/wjg.v18.i38.5321
c-Met in pancreatic cancer stem cells: Therapeutic implications
Marta Herreros-Villanueva, Aizpea Zubia-Olascoaga, Luis Bujanda
Marta Herreros-Villanueva, Division of Oncology Research, Department of Medicine, Schulze Center for Novel Therapeutics, Mayo Clinic, Rochester, MN 55905, United States
Aizpea Zubia-Olascoaga, IkerChem, Oncology Therapeutics Department, 20009 San Sebastian, Spain
Luis Bujanda, Department of Gastroenterology, Centro de Investigación Biomédica en Red en Enfermedades Hepáticas y Digestivas (CIBERehd), Donostia Hospital-Biodonostia Institute, University of the Basque Country, 20014 San Sebastian, Spain
Author contributions: Herreros-Villanueva M, Zubia-Olascoaga A and Bujanda L designed and wrote the review.
Correspondence to: Luis Bujanda, MD, PhD, Department of Gastroenterology, Centro de Investigación Biomédica en Red en Enfermedades Hepáticas y Digestivas (CIBERehd), Donostia Hospital-Biodonostia Institute, University of the Basque Country, 20014 San Sebastian, Spain. luis.bujanda@osakidetza.net
Telephone: +34-94-3007173 Fax: +34-94-3007065
Received: June 29, 2012
Revised: August 1, 2012
Accepted: August 3, 2012
Published online: October 14, 2012
Abstract

Pancreatic cancer is the deadliest solid cancer and currently the fourth most frequent cause of cancer-related deaths. Emerging evidence suggests that cancer stem cells (CSCs) play a crucial role in the development and progression of this disease. The identification of CSC markers could lead to the development of new therapeutic targets. In this study, the authors explore the functional role of c-Met in pancreatic CSCs, by analyzing self-renewal with sphere assays and tumorigenicity capacity in NOD SCID mice. They concluded that c-Met is a novel marker for identifying pancreatic CSCs and c-Methigh in a higher tumorigenic cancer cell population. Inhibition of c-Met with XL184 blocks self-renewal capacity in pancreatic CSCs. In pancreatic tumors established in NOD SCID mice, c-Met inhibition slowed tumor growth and reduced the population of CSCs, along with preventing the development of metastases.

Keywords: Cancer stem cells; c-Met; Gemcitabine; Self-renewal; Tumorigenicity