IGF2BP3-induced activation of EIF5B contributes to progression ofhepatocellular carcinoma cells br

In this study, we investigated the functional role of eukaryotic initiation factor 5B (EIF5B) in hepatocellularcarcinoma (HCC) and the underlying mechanisms. Bioinformatics analysis demonstrated that the EIF5B transcriptand protein levels as well as the EIF5Bcopy number were significantly higher in the HCC tissues compared with thenon-cancerous liver tissues. Down-regulation of EIF5B significantly decreased proliferation and invasiveness of theHCC cells. Furthermore, EIF5B knockdown suppressed epithelial-mesenchymal transition (EMT) and the cancer stemcell (CSC) phenotype. Down-regulation of EIF5B also increased the sensitivity of HCC cells to 5-fluorouracil (5-FU).In the HCC cells, activation of the NF-kappa B signaling pathway and IkB phosphorylation was significantly reducedby EIF5B silencing. IGF2BP3 increased the stability of the EIF5B mRNA in an m6A-dependent manner. Our datasuggested that EIF5B is a promising prognostic biomarker and therapeutic target in HCC