Review
Copyright ©The Author(s) 2015. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Hepatol. Oct 18, 2015; 7(23): 2459-2469
Published online Oct 18, 2015. doi: 10.4254/wjh.v7.i23.2459
Contribution of the toxic advanced glycation end-products-receptor axis in nonalcoholic steatohepatitis-related hepatocellular carcinoma
Jun-ichi Takino, Kentaro Nagamine, Takamitsu Hori, Akiko Sakasai-Sakai, Masayoshi Takeuchi
Jun-ichi Takino, Kentaro Nagamine, Takamitsu Hori, Department of Biochemistry, Faculty of Pharmaceutical Sciences, Hiroshima International University, Hiroshima 737-0112, Japan
Akiko Sakasai-Sakai, Masayoshi Takeuchi, Department of Advanced Medicine, Medical Research Institute, Kanazawa Medical University, Ishikawa 920-0293, Japan
Author contributions: All authors contributed to this study.
Supported by The Japan Society for the Promotion of Science (JSPS) KAKENHI, Grant No. 22300264 and No. 25282029 (to Takeuchi M); the Ministry of Education, Culture, Sports, Science; Technology (MEXT), Regional Innovation Strategy Support Program (to Takeuchi M); and Kanazawa Medical University, No. SR2012-04.
Conflict-of-interest statement: The authors declare no conflict of interest associated with this manuscript.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Correspondence to: Masayoshi Takeuchi, PhD, Department of Advanced Medicine, Medical Research Institute, Kanazawa Medical University, 1-1 Daigaku, Uchinada-machi, Kahoku, Ishikawa 920-0293, Japan. takeuchi@kanazawa-med.ac.jp
Telephone: +81-76-2862211 Fax: +81-76-2863652
Received: March 18, 2015
Peer-review started: March 18, 2015
First decision: April 23, 2015
Revised: May 7, 2015
Accepted: August 29, 2015
Article in press: September 7, 2015
Published online: October 18, 2015
Processing time: 215 Days and 3.8 Hours
Core Tip

Core tip: Expression of the receptor for advanced glycation end-products (RAGE), which is a multi-ligand cell surface receptor, is correlated with the poor therapeutic outcomes and malignancy of hepatocellular carcinoma (HCC). The synthesis of toxic advanced glycation end-products (TAGE), ligands of RAGE, is increased in nonalcoholic steatohepatitis (NASH) as well as in NASH-related HCC. Interactions between TAGE and RAGE induce oxidative stress, which may, in turn, lead to adverse effects in tumor cells and hepatic stellate cells during NASH or NASH-related HCC progression. Therefore, these findings prompted us to suggest that the TAGE-RAGE axis may be a treatment target in NASH-related HCC.