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Claudins, Inflammation and Epithelial-Mesenchymal Transition in Gastric Tissue
Rendon-Huerta E*, Chavarria-Velazquez CO and Montaño LFDepartment of Cell and Tissue Biology, Immunobiology Laboratory, UNAM, Mexico
- *Corresponding Author:
- Rendon-Huerta E
Faculty of Medicine, Department of Cell and Tissue Biology
Immunobiology Laboratory, UNAM, Mexico
E-mail: erendon@bq.unam.mx
Received date: September 26, 2013; Accepted date: October 26, 2013; Published date: November 02, 2013
Citation: Rendon-Huerta E, Chavarria-Velazquez CO, Montaño LF (2013) Claudins, Inflammation and Epithelial-Mesenchymal Transition in Gastric Tissue. J Gastroint Dig Syst 3:149. doi:10.4172/2161-069X.1000149
Copyright: © 2013 Rendon-Huerta E, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Abstract
Gastric cancer is a serious worldwide health burden. It is the fourth most frequently diagnosed cancer with an estimated 1 million new cases per year. The disease is often diagnosed in advanced stages and is associated with a poor prognosis for patients. It exhibits heterogeneity in clinical, biologic, and genetic aspects. Although H. pylori is the best studied risk factor, interleukins associated with chronic inflammation, disruption of tight junctions especially claudins, MERK/ERK signaling pathways and cancer stem cells have key roles in carcinogenesis and progression. An in-depth understanding of the role that inflammation and modified tight junction proteins play in epithelial-mesenchymal transition may improve our understanding of the cancer process and lead to the recognition of new biomarkers for early diagnosis, and possibly, improved therapeutics.
