Copyright
©The Author(s) 2016. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Sep 21, 2016; 22(35): 7938-7950
Published online Sep 21, 2016. doi: 10.3748/wjg.v22.i35.7938
Published online Sep 21, 2016. doi: 10.3748/wjg.v22.i35.7938
Therapeutic aspects of c-MYC signaling in inflammatory and cancerous colonic diseases
Ferenc Sipos, Gábor Firneisz, Györgyi Műzes, 2nd Department of Internal Medicine, Semmelweis University, H-1088 Budapest, Hungary
Author contributions: Sipos F, Firneisz G and Műzes G contributed to the writing, editing and revising of this paper.
Conflict-of-interest statement: All authors declare no conflict of interest.
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: Ferenc Sipos, MD, PhD, 2nd Department of Internal Medicine, Semmelweis University, Szentkirályi Street 46., H-1088 Budapest, Hungary. dr.siposf@gmail.com
Telephone: +36-1-2660926 Fax: +36-1-2660816
Received: July 7, 2016
Peer-review started: July 11, 2016
First decision: July 29, 2016
Revised: August 4, 2016
Accepted: August 23, 2016
Article in press: August 23, 2016
Published online: September 21, 2016
Processing time: 68 Days and 20.1 Hours
Peer-review started: July 11, 2016
First decision: July 29, 2016
Revised: August 4, 2016
Accepted: August 23, 2016
Article in press: August 23, 2016
Published online: September 21, 2016
Processing time: 68 Days and 20.1 Hours
Core Tip
Core tip: The c-MYC gene is frequently deregulated in colonic inflammation, and overexpressed in both sporadic and colitis-associated colon adenocarcinomas. Endogenous c-MYC is essential for efficient induction of p53-dependent apoptosis following DNA damage, moreover its function is also involved in and regulated by autophagy-related mechanisms, and its expression is affected by DNA-methylation, or histone acetylation. Increasing our knowledge about MYC-dependent pathways might provide direction to novel colonic anti-inflammatory and anti-cancer strategies.