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©2014 Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Dec 21, 2014; 20(47): 17699-17708
Published online Dec 21, 2014. doi: 10.3748/wjg.v20.i47.17699
Published online Dec 21, 2014. doi: 10.3748/wjg.v20.i47.17699
Toll-like receptor signaling in colorectal cancer: Carcinogenesis to cancer therapy
Ting-Ting Li, Department of Geriatric Gastroenterology, Chinese PLA General Hospital, Beijing 100853, China
Ting-Ting Li, Shuji Ogino, Zhi Rong Qian, Department of Medical Oncology, Dana-Farber Cancer Institute and Harvard Medical School, Boston, MA 02215, United States
Shuji Ogino, Department of Pathology, Brigham and Women’s Hospital and Harvard Medical School, Boston, MA 02215, United States
Shuji Ogino, Department of Epidemiology, Harvard School of Public Health, Boston, MA 02215, United States
Author contributions: Li TT and Qian ZR contributed equally to this paper; Li TT and Qian ZR did problem formulation; Li TT performed literature search and wrote the paper; Qian ZR and Ogino S revised the manuscript.
Supported by grant from United States National Institute of Health (NIH), No. P01 CA87969 (to SE Hankinson), No. UM1 CA167552, and No. P01 CA55075 (to WC Willett), No. R01 CA137178 (to AT Chan), No. P50 CA127003 (to CS Fuchs), No. R01 CA151993 (to S Ogino); Bennett Family Fund for Targeted Therapies Research; and Entertainment Industry Foundation through National Colorectal Cancer Research Alliance
Correspondence to: Zhi Rong Qian, MD, PhD, Department of Medical Oncology, Dana-Farber Cancer Institute and Harvard Medical School, 450 Brookline Ave., Room M420, Boston, MA 02215, United States. zhirong_qian@dfci.harvard.edu
Telephone: +1-617-5829145 Fax: +1-617-5828558
Received: May 28, 2014
Revised: August 27, 2014
Accepted: November 18, 2014
Published online: December 21, 2014
Revised: August 27, 2014
Accepted: November 18, 2014
Published online: December 21, 2014
Core Tip
Core tip: Toll-like receptors (TLRs) are innate immune sensors which can recognize inflammatory mediators. TLRs have been shown to mediate inflammatory response and maintain epithelial barrier homeostasis. Inflammation is a risk factor for many cancers including colorectal cancer (CRC). The key molecules involved in inflammation-driven carcinogenesis include TLRs. In this paper, we reviewed TLR signaling in CRC from carcinogenesis to cancer therapy.