Li J, Sun X, He P, Liu WQ, Zou YB, Wang Q, Meng XW. Ubiquitin-like modifier activating enzyme 2 promotes cell migration and invasion through Wnt/β-catenin signaling in gastric cancer. World J Gastroenterol 2018; 24(42): 4773-4786 [PMID: 30479464 DOI: 10.3748/wjg.v24.i42.4773]
Corresponding Author of This Article
Xiang-Wei Meng, MD, Chief Doctor, Professor, Department of Gastroenterology, The First Hospital of Jilin University, No. 71 Xinmin Street, Changchun 130021, Jilin Province, China. mengxw@jlu.edu.cn
Research Domain of This Article
Gastroenterology & Hepatology
Article-Type of This Article
Basic Study
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. Nov 14, 2018; 24(42): 4773-4786 Published online Nov 14, 2018. doi: 10.3748/wjg.v24.i42.4773
Ubiquitin-like modifier activating enzyme 2 promotes cell migration and invasion through Wnt/β-catenin signaling in gastric cancer
Ji Li, Xun Sun, Ping He, Wan-Qi Liu, Ya-Bin Zou, Quan Wang, Xiang-Wei Meng
Ji Li, Ping He, Wan-Qi Liu, Xiang-Wei Meng, Department of Gastroenterology, The First Hospital of Jilin University, Changchun 130021, Jilin Province, China
Xun Sun, Ya-Bin Zou, Department of Pathology, The First Hospital of Jilin University, Changchun 130021, Jilin Province, China
Quan Wang, Gastrointestinal Surgery, The First Hospital of Jilin University, Changchun 130021, Jilin Province, China
Author contributions: Meng XW designed and coordinated the research; Li J performed the majority of experiments and wrote the paper; Sun X and Zou YB performed the immunohistochemistry; He P and Liu WQ analyzed the data; Wang Q performed the Western blot of the tissues.
Supported bythe Science and Technology Department of Jilin Province (No. 20150204006YY).
Institutional review board statement: This study was approved by the ethics committee of The First Hospital of Jilin University.
Conflict-of-interest statement: No potential conflicts of interest were disclosed.
Data sharing statement: Data are available from the first author at 492264624@qq.com.
ARRIVE guidelines statement: The authors have read the ARRIVE guidelines, and the manuscript was prepared and revised according to the ARRIVE guidelines.
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: Xiang-Wei Meng, MD, Chief Doctor, Professor, Department of Gastroenterology, The First Hospital of Jilin University, No. 71 Xinmin Street, Changchun 130021, Jilin Province, China. mengxw@jlu.edu.cn
Telephone: +86-431-85619183 Fax: +86-431-85619183
Received: August 7, 2018 Peer-review started: August 8, 2018 First decision: August 24, 2018 Revised: September 3, 2018 Accepted: October 5, 2018 Article in press: October 5, 2018 Published online: November 14, 2018 Processing time: 98 Days and 0.1 Hours
ARTICLE HIGHLIGHTS
Research background
Gastric cancer (GC) is the fourth most common malignancy and the second leading cause of cancer-related death globally. Although decreasing trends have been observed in GC incidence and mortality rates due to recent advances in diagnosis and treatment, the burden remains the highest in East Asia (especially in China). However, many GC patients are already at an inoperable advanced stage at diagnosis, which results in poor outcome. Thus, new therapeutic targets that may confer survival benefit are urgently needed in GC.
Research motivation
There are insufficient reports about the function and mechanism of ubiquitin-like modifier activating enzyme 2 (Uba2) in GC migration, epithelial-mesenchymal transition, and invasion.
Research objectives
The aim of this study is to investigate the role of Uba2 in GC migration and invasion, and its underlying mechanism.
Research methods
Uba2 expression was examined at the protein level by immunohistochemistry or Western blotting in tissues and cells. Correlations of Uba2 expression and clinicopathological characteristics were also analyzed. Transwell and wound healing assays were used to examine the effects of Uba2 on GC migration and invasion. Western blotting and luciferase reporter assay were used to investigate the underlying mechanism.
Research results
The up-regulation of Uba2 expression was found in both GC tissues and cells. Knock-down of Uba2 inhibited cell proliferation, migration and invasion, and over-expression of Uba2 showed the opposite effects. Wnt/β-catenin signaling might be involved in the oncogenic function of Uba2.
Research conclusions
The study shows that Uba2 is an enhancer of cell migration and invasion in GC, and the possible mechanism is via regulating the canonical Wnt signaling pathway and enhancing epithelial-mesenchymal transition. Thus, Uba2 is expected to be an important oncoprotein and potential therapeutic target in GC.
Research perspectives
The function and mechanism of Uba2 in GC development has been confirmed, and the significance of Uba2 as a promising therapeutic target for GC is highlighted.
