Yang LY, Song GL, Zhai XQ, Wang L, Liu QL, Zhou MS. MicroRNA-331 inhibits development of gastric cancer through targeting musashi1. World J Gastrointest Oncol 2019; 11(9): 705-716 [PMID: 31558975 DOI: 10.4251/wjgo.v11.i9.705]
Corresponding Author of This Article
Ming-Shun Zhou, PhD, Professor, Department of Emergency, Second Affiliated Hospital of Shandong First Medical University, Taian 271016, Shandong Province, China. zhoumingshun790@163.com
Research Domain of This Article
Cell Biology
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/
Lei-Ying Yang, Li Wang, Qin-Lai Liu, Department of Pathology, Shandong First Medical University, Taian 271016, Shandong Province, China
Guang-Le Song, Morphological Laboratory, Shandong First Medical University, Taian 271016, Shandong Province, China
Xiao-Qian Zhai, Department of Pathology, Second Affiliated Hospital of Shandong First Medical University, Taian 271016, Shandong Province, China
Ming-Shun Zhou, Department of Emergency, Second Affiliated Hospital of Shandong First Medical University, Taian 271016, Shandong Province, China
Author contributions: Zhou MS designed research; Yang LY, Song GL, Zhai XQ, Wang L and Liu QL performed research; Yang LY analyzed data; Yang LY and Zhou MS wrote the paper.
Institutional animal care and use committee statement: The study was approved by the Institutional Animal Care and Use Committee of Affiliated Hospital Taishan Medical University.
Conflict-of-interest statement: The authors declare no conflict of interest.
Data sharing statement: No additional data are available.
ARRIVE guidelines statement: The ARRIVE Guidelines have been adopted.
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/
Corresponding author: Ming-Shun Zhou, PhD, Professor, Department of Emergency, Second Affiliated Hospital of Shandong First Medical University, Taian 271016, Shandong Province, China. zhoumingshun790@163.com
Telephone: +86-538-6998075Fax: +86-538-6998075
Received: March 17, 2019 Peer-review started: March 18, 2019 First decision: March 28, 2019 Revised: April 10, 2019 Accepted: July 16, 2019 Article in press: July 17, 2019 Published online: September 15, 2019 Processing time: 181 Days and 1.5 Hours
ARTICLE HIGHLIGHTS
Research background
As one of the most frequent cancers, gastric cancer (GC) caused more than 700000 deaths in just 2012 worldwide. Although the molecular mechanisms involved in microRNAs (miRNAs) have been extensively investigated in GC, how miR-331 regulates GC pathogenesis remains unknown.
Research motivation
To find more molecular mechanism or biomarker for diagnosis and treatment of GC
Research objectives
This study aims to explore the anti-cancer effect of miR-331 in GC and investigate its molecular mechanism against GC cells.
Research methods
MiR-331 expression was observed by qRT-PCR assay in GC tissues and cell lines. MiR-331 mimic or inhibitor was transfected into MKN-45 cells to perform gain-loss experiment to observe effect of miR-331 on GC cell viability and migration. Bioinformatics analysis is used to predict the target gene of miR-331. The antagonistic effect between and MSI1 was confirmed by gain-loss experiment and detection of proliferation and migration. The expression of crucial proteins was measured by western blotting.
Research results
We found that downregulation of miR-331 was associated with poor prognosis in GC. In addition, miR-331 significantly inhibited GC cell growth, migration and invasion. Further, MSI1 was verified to directly target miR-331 and can effectively be regulated in GC tissues. Furthermore, upregulation of MSI1 weakened the inhibitory effect of miR-331 in GC. Western blotting analysis showed that E-cadherin, N-cadherin and Vimentin expression markedly affected by miR-331 and MSI1 in GC cell line, suggesting that EMT is a very direct regulated target of miR-331 and MSI1 in GC.
Research conclusions
Our study demonstrated that miR-331 can significantly inhibit GC cell growth, migration and invasion. Furthermore, it can work through MSI1. Therefore, our study provides some molecular mechanism and two new biomarkers for GC.
Research perspectives
In the future, research may reveal the important role of miR-331 that enhances the sensitivity of GC detection and further develop for its application in anti-cancer treatments. The identification of the miR-331/MSI1 molecular axis may further explain the underlying mechanism.
