MiR-92b promotes gastric cancer growth by activating the DAB2IP-mediated PI3K/AKT signalling pathway.

Abstract

ObjectivesmiR‐92b has been reported to play critical roles in several carcinomas; however, our understanding of the mechanisms by which miR‐92b stimulates gastric cancer (GC) is incomplete. The aim of this study was to investigate the clinical significance and functional relevance of miR‐92b in GC.Materials and methodsExpression of miR‐92b in GC and peritumoural tissues was determined using qRT‐PCR, in situ hybridization and bioinformatics. CCK‐8, colony formation and fluorescence‐activated cell sorting assays were utilized to explore the effect of miR‐92b on GC cells. A luciferase reporter assay and Western blotting were employed to verify miR‐92b targeting of DAB2IP. Furthermore, Western blotting was used to evaluate the levels of DAB2IP and PI3K/Akt signalling pathway‐related proteins.ResultsIn this study, we found that miR‐92b was upregulated in GC tissues compared with peritumoural tissues. Overexpression of miR‐92b promoted cell proliferation, colony formation, and G0/G1 transition and decreased apoptosis. Our results indicated that miR‐92b repressed the expression of DAB2IP and that loss of DAB2IP activated the PI3K/AKT signalling pathway. Overexpression of DAB2IP rescued the effects of miR‐92b in GC cells. Finally, our results demonstrated a significant correlation between miR‐92b expression and DAB2IP expression in GC tissues.ConclusionsOur results suggest that miR‐92b promotes GC cell proliferation by activating the DAB2IP‐mediated PI3K/AKT signalling pathway. The miR‐92b/DAB2IP/PI3K/AKT signalling axis may be a potential therapeutic target to prevent GC progression.