Published online Dec 7, 2019. doi: 10.3748/wjg.v25.i45.6619
Peer-review started: September 5, 2019
First decision: October 14, 2019
Revised: October 29, 2019
Accepted: November 13, 2019
Article in press: November 13, 2019
Published online: December 7, 2019
Gastric cancer (GC) has become a serious threat to people's health. Accumulative evidence reveals that dysregulation of numerous microRNAs (miRNAs) has been found during malignant formation. So far, the role of microRNA-760 (miR-760) in the development of GC is largely unknown.
To measure the expression level of miR-760 in GC and investigate its role in gastric tumorigenesis.
Real-time quantitative polymerase chain reaction and Western blot analysis were used to measure the expression of miR-760 and G-protein-coupled receptor kinase interacting protein-1 (GIT1). Cell growth was detected by 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) and cell colony formation assays. Apoptosis was assessed by flow cytometric analysis. The relationship between miR-760 and GIT1 was verified by luciferase reporter assay.
The results showed that the expression of miR-760 was decreased in GC and associated with poor clinical outcomes in GC patients. Furthermore, miR-760 restrained cell proliferation and cell colony formation and induced apoptosis in GC cells. In addition, miR-760 directly targeted GIT1 and negatively regulated its expression in GC. GIT1 was upregulated in GC and predicted a worse prognosis in GC patients. We also found that upregulation of GIT1 weakened the inhibitory effect of miR-760 in GC.
In conclusion, miR-760 targets GIT1 to inhibit cell growth and promote apoptosis in GC cells. Our data demonstrate that miR-760 may be a potential target for the treatment of GC.
Core tip: The expression of microRNA-760 (miR-760) was decreased in gastric cancer (GC), which was related to poor clinical outcomes in GC patients. MiR-760 restrained cell proliferation and cell colony formation and induced cell apoptosis in GC cells. MiR-760 directly targets G-protein-coupled receptor kinase interacting protein-1 that is involved in tumorigenesis of GC.