miR-450b-5p loss mediated KIF26B activation promoted hepatocellular carcinoma progression by activating PI3K/AKT pathway

Abstract Background Kinesin family member 26B (KIF26B) is unveiled acted as important role in many solid tumors, however, the function of KIF26B in hepatocellular carcinoma (HCC) is unclear. Methods The expression of KIF26B in HCC tissues and cell lines were measured with immunochemistry, real-time PCR and western blotting. The correlation between KIF26B expression and clinicopathological characteristics were analyzed by SPSS19.0. Functional experiments of KIF26B was conducted by CCK-8, transwell, EDU, colony formation in vitro and tumorigenesis in vivo. The gene set enrichment analysis was used to search the downstream pathway, luciferase reporter experiment was used to find the upstream regulatory factor of KIF26B. Results In this study, we found that KIF26B was overexpressed both in HCC tissues and cell lines. High expression of KIF26B was associated with poor overall survival (OS), late TNM stage and poor differentiation. Loss of function experiments showed that suppression of KIF26B could inhibit cell viability, proliferation rate and invasion ability of HCC cells. KEGG and GO analysis showed that expression of KIF26B was highly relevant with PI3K/AKT signal pathway, and suppression of KIF26B could decrease the expression of m-TOR, p-PI3K and p-AKT. Further study demonstrated that expression of KIF26B was negative correlated with miR-450b-5p level in HCC tissues, and miR-450b-5p could inhibit cell viability, proliferation rate and invasion ability of HCC cells via targeted inhibiting KIF26B. Conclusion Our study demonstrated that miR-450-5p/KIF26B/AKT axis is critical for progression of HCC, and might provide novel prognostic biomarker and therapeutic target for HCC.