MiR-181b-5p facilitates proliferation and migration by regulating GSKIP through ERK/AKT signaling pathways in gastric cancer.

Gastric cancer (GC) is one of the most common malignant neoplasms. This study aims to explore the effects of miR-181b-5p on the proliferation and metastasis of GC and its potential molecular mechanisms. 5-Ethynyl-2'-deoxyuridine (EdU), cell counting kit-8 (CCK8), and flow cytometry assay were used to assess the proliferation. Transwell and wound-healing assay were performed to evaluate the migration ability. Dual luciferase reporter assay, quantitative real-time PCR (qRT-PCR) and western blotting were used to validate that Glycogen synthase kinase 3β interaction protein (GSKIP) was the target gene of miR-181b-5p. Tumor formation in NTG mice was applied to determine the effects of miR-181b-5p on cell proliferation in vivo. In this study, we showed that miR-181b-5p promoted the proliferation and migration in vitro and facilitated GC growth in vivo. Mechanistically, we confirmed that miR-181b-5p accelerated tumor progression by targeting GSKIP. Furthermore, we found that miR-181b-5p overexpression activated the Erk/AKT signaling pathway through downregulating GSKIP. Taken together, miR-181b-5p had a role in causing cancer, which suggested that it could be used as a target for treatment in GC.