Tanabe S, Aoyagi K, Yokozaki H, Sasaki H. Regulation of CTNNB1 signaling in gastric cancer and stem cells. World J Gastrointest Oncol 2016; 8(8): 592-598 [PMID: 27574551 DOI: 10.4251/wjgo.v8.i8.592]
Corresponding Author of This Article
Shihori Tanabe, PhD, Division of Risk Assessment, Biological Safety Research Center, National Institute of Health Science, 1-18-1, Kami-yoga, Setagaya-ku, Tokyo 158-8501, Japan. stanabe@nihs.go.jp
Research Domain of This Article
Gastroenterology & Hepatology
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/
Shihori Tanabe, Division of Risk Assessment, Biological Safety Research Center, National Institute of Health Science, Tokyo 158-8501, Japan
Kazuhiko Aoyagi, Hiroki Sasaki, Department of Translational Oncology, National Cancer Center Research Institute, Tokyo 104-0045, Japan
Hiroshi Yokozaki, Department of Pathology, Kobe University of Graduate School of Medicine, Kobe 650-0017, Japan
Author contributions: Tanabe S wrote the paper; Aoyagi K, Yokozaki H and Sasaki H contributed critical revisions of the manuscript for important intellectual content.
Conflict-of-interest statement: The authors declare that no conflicts of interest exist.
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: Shihori Tanabe, PhD, Division of Risk Assessment, Biological Safety Research Center, National Institute of Health Science, 1-18-1, Kami-yoga, Setagaya-ku, Tokyo 158-8501, Japan. stanabe@nihs.go.jp
Telephone: +81-3-37001141 Fax: +81-3-37076950
Received: March 7, 2016 Peer-review started: March 7, 2016 First decision: April 18, 2016 Revised: April 22, 2016 Accepted: May 17, 2016 Article in press: May 27, 2016 Published online: August 15, 2016 Processing time: 154 Days and 15.5 Hours
Abstract
Recent research has shown that the alteration of combinations in gene expression contributes to cellular phenotypic changes. Previously, it has been demonstrated that the combination of cadherin 1 and cadherin 2 expression can identify the diffuse-type and intestinal-type gastric cancers. Although the diffuse-type gastric cancer has been resistant to treatment, the precise mechanism and phenotypic involvement has not been revealed. It may be possible that stem cells transform into gastric cancer cells, possibly through the involvement of a molecule alteration and signaling mechanism. In this review article, we focus on the role of catenin beta 1 (CTNNB1 or β-catenin) and describe the regulation of CTNNB1 signaling in gastric cancer and stem cells.
Core tip: CTNNB1 signaling is essential for revealing cancer mechanisms. The molecular dynamism in stem cells and cancer is illustrated with a pathway cascade. The CTNNB1 protein interacts with signaling molecules upon stimulation, leading to the transcription of genes related to cell proliferation. Mutations of signaling molecules are also important factors for cancer development. CTNNB1 signaling in stem cells and cancer are mainly described in the article.
