ArticleOncology research2022
IGF2BP3-induced activation of EIF5B contributes to progression of hepatocellular carcinoma cells.
Article in Oncology research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 13 citations in OpenAlex.
- NF-κB signaling in hepatocellular carcinoma: Mechanisms of tumor progression, immune evasion, and therapeutic resistance.Translational oncology · 2026Review
- Synovial transcriptome analysis reveals ShenTong ZhuYu Tang alleviates osteoarthritis by targeting MMP-9 and immune microenvironment.Journal of orthopaedic surgery and research · 2026Article
- Deciphering the crucial role of IGF2BP3 in modulating stemness traits of salivary adenoid cystic carcinoma.Medical oncology (Northwood, London, England) · 2025Article
- ElF5B as a prognostic biomarker and its correlation with infiltrating immune cells in liver cancer.Genes & genomics · 2025Article
- FOXM1-activated IGF2BP3 promotes cell malignant phenotypes and M2 macrophage polarization in hepatocellular carcinoma by inhibiting ferroptosis via stabilizing RRM2 mRNA in an m6A-dependent manner.Molecular and cellular biochemistry · 2025Article
- Nitidine chloride inhibits the progression of hepatocellular carcinoma by suppressing IGF2BP3 and modulates metabolic pathways in an mMolecular medicine (Cambridge, Mass.) · 2025Article
- Splicing factor PTBP1 promotes hepatocarcinogenesis via oncogenic splice-switching of MAPT.Oncology research · 2025Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In this study, we investigated the functional role of eukaryotic initiation factor 5B (EIF5B) in hepatocellular carcinoma (HCC) and the underlying mechanisms. Bioinformatics analysis demonstrated that the EIF5B transcript and protein levels as well as the EIF5Bcopy number were significantly higher in the HCC tissues compared with the non-cancerous liver tissues. Down-regulation of EIF5B significantly decreased proliferation and invasiveness of the HCC cells. Furthermore, EIF5B knockdown suppressed epithelial-mesenchymal transition (EMT) and the cancer stem cell (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 reduced by EIF5B silencing. IGF2BP3 increased the stability of the EIF5B mRNA in an m6A-dependent manner. Our data suggested that EIF5B is a promising prognostic biomarker and therapeutic target in HCC.
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