Gambhir S, Vyas D, Hollis M, Aekka A, Vyas A. Nuclear factor kappa B role in inflammation associated gastrointestinal malignancies. World J Gastroenterol 2015; 21(11): 3174-3183 [PMID: 25805923 DOI: 10.3748/wjg.v21.i11.3174]
Corresponding Author of This Article
Dinesh Vyas, MD, MS, FICS, FACS, Department of Surgery, College of Human Medicine, Michigan State University, 1200 East Michigan Avenue, Suite 655, East Lansing, MI 48912, United States. dinesh.vyas@hc.msu.edu
Research Domain of This Article
Biology
Article-Type of This Article
Review
Open-Access Policy of This Article
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/
World J Gastroenterol. Mar 21, 2015; 21(11): 3174-3183 Published online Mar 21, 2015. doi: 10.3748/wjg.v21.i11.3174
Nuclear factor kappa B role in inflammation associated gastrointestinal malignancies
Sahil Gambhir, Dinesh Vyas, Michael Hollis, Apporva Aekka, Arpita Vyas
Sahil Gambhir, Dinesh Vyas, Michael Hollis, Apporva Aekka, Department of Surgery, College of Human Medicine, Michigan State University, East Lansing, MI 48912, United States
Arpita Vyas, Department of Pediatrics, College of Human Medicine - Michigan State University, East Lansing, MI 48912, United States
Author contributions: Gambhir S and Vyas D contributed equally to this work; Gambhir S and Vyas D designed research; analyzed data and wrote the paper; Hollis M contributed in research and editing; Vyas A contributed in data and conceptualization; Aekka A contributed in editing.
Conflict-of-interest: No potential conflicts of interest relevant to this article were reported.
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: Dinesh Vyas, MD, MS, FICS, FACS, Department of Surgery, College of Human Medicine, Michigan State University, 1200 East Michigan Avenue, Suite 655, East Lansing, MI 48912, United States. dinesh.vyas@hc.msu.edu
Telephone: +-517-2672491 Fax: +1-517-2672488
Received: June 15, 2014 Peer-review started: June 16, 2014 First decision: August 15, 2014 Revised: August 29, 2014 Accepted: February 12, 2015 Article in press: February 13, 2015 Published online: March 21, 2015
Abstract
Nuclear factor kappa B (NF-κB) has an established role in the regulation of innate immunity and inflammation. NF-κB is also involved in critical mechanisms connecting inflammation and cancer development. Recent investigations suggest that the NF-κB signaling cascade may be the central mediator of gastrointestinal malignancies including esophageal, gastric and colorectal cancers. This review will explore NF-κB’s function in inflammation-associated gastrointestinal malignancies, highlighting its oncogenic contribution to each step of carcinogenesis. NF-κB’s role in the inflammation-to-carcinoma sequence in gastrointestinal malignancies warrants stronger emphasis upon targeting this pathway in achieving greater therapeutic efficacy.
Core tip: Inflammation has a critical role in cancer, its metastasis and angiogenesis. One of the critical mediator is nuclear transcription factor nuclear factor kappa B. This article will be critically useful for basic scientist and clinicians in understanding the the importance of this transcription factor.
