J Cancer 2015; 6(8):694-700. doi:10.7150/jca.11709
Genes Regulating Epithelial Polarity Are Critical Suppressors of Esophageal Oncogenesis
1. Center for Cancer Research, Xinxiang Medical University, Xinxiang Henan, 453003, China.
2. Ontario Cancer Institute, Campbell Family Institute for Breast Cancer Research, University of Toronto, Toronto, Ontario, M5G 2M9, Canada.
3. Department of Cellular and Molecular Biology, University of Texas Health Science Center at Tyler, Tyler, Texas, 75708, USA
4. Texas Lung Injury Institute, University of Texas Health Science Center at Tyler, Tyler, Texas, 75708, USA.
Li XM, Wang H, Zhu LL, Zhao RZ, Ji HL. Genes Regulating Epithelial Polarity Are Critical Suppressors of Esophageal Oncogenesis. J Cancer 2015; 6(8):694-700. doi:10.7150/jca.11709. Available from http://www.jcancer.org/v06p0694.htm
Esophageal cancer is an aggressive disease featured by early lymphatic and hematogenous dissemination, and is the sixth leading cause of cancer-related deaths worldwide. The proper formation of apicobasal polarity is essential for normal epithelium physiology and tissue homeostasis, while loss of polarity is a hallmark of cancer development including esophageal oncogenesis. In this review, we summarized the stages of esophageal cancer development associated with the loss or deregulation of epithelial cell apicobasal polarity. Loss of epithelial apicobasal polarity exerts an indispensable role in the initiation of esophageal oncogenesis, tumor progression, and the advancement of tumors from benign to malignant. In particular, we reviewed the involvement of several critical genes, including Lkb1, claudin-4, claudin-7, Par3, Lgl1, E-cadherin, and the Scnn1 gene family. Understanding the role of apicobasal regulators may lead to new paradigms for treatment of esophageal tumors, including improvement of prognostication, early diagnosis, and individually tailored therapeutic interventions in esophageal oncology.
Keywords: apicobasal polarity, esophageal adenocarcinoma, esophageal squamous cell carcinoma, LKB1, LGL1, SCNN1