Objective: To investigate the expression, clinical significance and biological function of miR-105-5p in gastric cancer (GC), as well as its potential action mechanism.
Methods: The expressions of miR-105-5p in GC and tumor adjacent tissues as well as in different GC cell lines (MGC 803, MKN 1, SGC 7901, BGC 823 and AGS) and normal gastric mucosal cell line (GES-1) were determined by real-time PCR. The relations of miR-105-5p expression with the clinicopathologic features and prognosis of GC patients were analyzed. The effects of miR-105-5p on migration, invasion and proliferation of GC cells were examined by Transwell migration and invasion assay and MTT assay, respectively. The potential target gene for miR-105-5p was predicted by using Bioinformatics tools, and then, the correlation between miR-105-5p and its target gene was verified by Luciferase reporter assay and Western blot, respectively. 
Results: The expression of miR-105-5p in GC tissues was significantly higher than that in tumor adjacent tissue, and in each studied GC cell line was significantly higher than that in normal gastric mucosal cell line (all P<0.05). The expression of miR-105-5p was significantly associated with tumor size (P=0.020) and distant metastasis (P=0.004); the overall survival rate in GC patients with low miR-105-5p expression was significantly higher than that in GC patients with high miR-105-5p expression (P=0.001 8). The BGC-823 cells with a relatively low miR-105-5p expression and the MKN 1 cells with a relatively high miR-105-5p expression were transfected with miR-105-5p mimics and miR-105-5p inhibitors respectively, and the results after transfection showed that the migration, invasion and proliferative abilities in BGC-823 cells were significantly increased, while were significantly decreased in MKN 1 cells (all P<0.05). Bioinformatics analysis suggested that DIRAS family GTPase 3 (DIRAS3) was possibly be the target of miR-105-5p; luciferase reporter assay indicated that the luciferase activity of DIRAS3-3’-UTR was negatively regulated by miR-105-5p; Western blot demonstrated that the DIRAS3 expression was significantly down-regulated in BGC-823 after transfection with miR-105-5p mimics, and was significantly up-regulated in MKN 1 cells after transfection with miR-105-5p inhibitors (both P<0.05).
Conclusion: The expression of miR-105-5p is elevated in GC, promotes migration, which can enhance the migration, invasion and proliferative abilities of GC cells probably through targeting DIRAS3, and thereby promote the occurrence and development of GC.