Published online Sep 15, 2019. doi: 10.4251/wjgo.v11.i9.705
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
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.
To find more molecular mechanism or biomarker for diagnosis and treatment of GC
This study aims to explore the anti-cancer effect of miR-331 in GC and investigate its molecular mechanism against GC cells.
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.
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.
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.
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.