Potential role of chitinase 3-like-1 in inflammation-associated carcinogenic changes of epithelial cells

作     者：Katrin Eurich Mayuko Segawa Satoko Toei-Shimizu Emiko Mizoguchi 

作者机构：Gastrointestinal UnitDepartment of MedicineMassachusetts General HospitalHarvard Medical SchoolBostonMA 02114United States Center for the Study of Inflammatory Bowel DiseaseMassachusetts General HospitalHarvard Medical SchoolBostonMA 02114United States 

出 版 物：《World Journal of Gastroenterology》 (世界胃肠病学杂志（英文版）)

年 卷 期：2009年第15卷第42期

页      面：5249-5259页

核心收录：

学科分类：1002[医学-临床医学] 100214[医学-肿瘤学] 10[医学] 

基　　金：Supported by NIH (DK64289,DK74454,DK43351 and DK80070) grants from the Eli and Edythe L.Broad Medical Foundation American Gastroenterological Association Foundation for Digestive Health and Nutrition to Mizoguchi E 

主　　题：Mammals Chitinase 3-1ike 1 Colon Epithelial cells Inflammation Colitis Colon neoplasms Inflammatory bowel disease 

摘      要：The family of mammalian chitinases includes members both with and without glycohydrolase enzymatic activity against chitin, a polymer of N-acetylglucosamine. Chitin is the structural component of fungi, crustaceans, insects and parasitic nematodes, but is completely absent in mammals. Exposure to antigens containing chitin- or chitin-like structures sometimes induces strong T helper type-I responses in mammals, which may be associated with the induction of mammalian chitinases. Chitinase 3-like-1 （CHI3L1）, a member of the mammalian chitinase family, is induced specifically during the course of inflammation in such disorders as inflammatory bowel disease, hepatitis and asthma. In addition, CHI3L1 is expressed and secreted by several types of solid tumors including glioblastoma, colon cancer, breast cancer and malignant melanoma. Although the exact function of CHI3L1 in inflammation and cancer is still largely unknown, CHI3L1 plays a pivotal role in exacerbating the inflammatory processes and in promoting angiogenesis and remodeling of the extracellular matrix. CHI3L1 may be highly involved in the chronic engagement of inflammation which potentiates development of epithelial tumorigenesis presumably by activating the mitogen-activated protein kinase and the protein kinase B signaling pathways. Anti-CHI3L1 antibodies or pan-chitinase inhibitors may have the potential to suppress CHI3Ll-mediated chronic inflammation and the subsequent carcinogenic change in epithelial cells.