期刊
WORLD JOURNAL OF GASTROENTEROLOGY
卷 20, 期 31, 页码 10813-10824出版社
BAISHIDENG PUBLISHING GROUP INC
DOI: 10.3748/wjg.v20.i31.10813
关键词
Tight junctions; Claudins; Tricellulin; MarvelD3; Normal human pancreatic duct epithelial cells; Pancreatic cancer; Protein kinase C; Epithelial to mesenchymal transition
资金
- Ministry of Education, Culture, Sports Science, and Technology
- Ministry of Health, Labour and Welfare of Japan
Pancreatic cancer continues to be a leading cause of cancer-related death worldwide and there is an urgent need to develop novel diagnostic and therapeutic strategies to reduce the mortality of patients with this disease. In pancreatic cancer, some tight junction proteins, including claudins, are abnormally regulated and therefore are promising molecular targets for diagnosis, prognosis and therapy. Claudin-4 and -18 are overexpressed in human pancreatic cancer and its precursor lesions. Claudin-4 is a high affinity receptor of Clostridium perfringens enterotoxin (CPE). The cytotoxic effects of CPE and monoclonal antibodies against claudin-4 are useful as novel therapeutic tools for pancreatic cancer. Claudin-18 could be a putative marker and therapeutic target with prognostic implications for patients with pancreatic cancer. Claudin-1, -7, tricellulin and marvelD3 are involved in epithelial to mesenchymal transition (EMT) of pancreatic cancer cells and thus might be useful as biomarkers during disease. Protein kinase C is closely related to EMT of pancreatic cancer and regulates tight junctions of normal human pancreatic duct epithelial cells and the cancer cells. This review focuses on the regulation of tight junctions via protein kinase C during EMT in human pancreatic cancer for the purpose of developing new diagnostic and therapeutic modalities for pancreatic cancer. (C) 2014 Baishideng Publishing Group Inc. All rights reserved.
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