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
The molecular mechanisms involved in microRNAs (miRNAs) have been extensively investigated in gastric cancer (GC). However, how miR-331 regulates GC pathogenesis remains unknown.
To illuminate the effect of miR-331 on cell metastasis and tumor growth in GC.
The qRT-PCR, CCK8, Transwell, cell adhesion, Western blot, luciferase reporter and xenograft tumor formation assays were applied to explore the regulatory mechanism of miR-331 in GC.
Downregulation of miR-331 associated with poor prognosis was detected in GC. Functionally, miR-331 suppressed cell proliferation, metastasis and tumor growth in GC. Further, miR-331 was verified to directly target musashi1 (MSI1). In addition, miR-331 inversely regulated MSI1 expression in GC tissues. Furthermore, upregulation of MSI1 weakened the inhibitory effect of miR-331 in GC.
miR-331 inhibited development of GC through targeting MSI1, which may be used as an indicator for the prediction and prognosis of GC.
Core tip: Gastric cancer (GC) has become one of the main threats to human life and health. MicroRNAs (miRNAs) have been reported to act as promoters and inhibitors in GC. In this study, the effect of miR-331 on cell metastasis and tumor growth was illuminated in GC. The results showed that miR-331 was downregulated in GC, which predicted poor prognosis in GC patients. Moreover, overexpression of miR-331 inhibited cell metastasis and tumor growth in GC cells. Further, musashi1 (MSI1) is a direct target gene of miR-331. MiR-331 inhibited GC progression through the suppression of MSI1.