ArticlePloS one2026
IGF1/IGF-1R promotes hepatocellular carcinoma progression by activating the Akt/GSK-3β pathway.
Article in PloS one, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
2 citing papers in PubMed.
- Dioscin Reverses Drug Resistance via AKT/GSK3β-mediated P-gp Degradation and EMT Inhibition.Drug development research · 2026Article
- Evidence for a Potential Context-Dependent Dual Role of Eb Peptide of IGF-1Eb in Cancer Cell Survival and Adaptation to UV Stress.International journal of molecular sciences · 2026Article
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The incidence of hepatocellular carcinoma (HCC) is increasing each year, with challenges such as increasing drug resistance and a high post-treatment recurrence rate. Therefore, investigating the novel pathogenic mechanisms is warranted. In this study, we investigated novel molecular mechanisms that affect HCC progression. Immunofluorescence analysis, immunohistochemical staining, and immunoblotting were performed to assess elevated IGF-1R expression in HCC cells. The EdU incorporation and colony formation assays revealed that IGF-1R promotes HCC cell proliferation. Furthermore, wound healing and Transwell migration assays revealed that IGF-1R phosphorylation enhances the migration of HCC cells. In addition, JC-1 apoptosis assays revealed that IGF-1R inhibits HCC cell apoptosis. Immunoblotting was performed to assess the protein phosphorylation level of Akt/GSK-3β downstream of IGF1/IGF-1R to explore the molecular mechanism. IGF-1R expression was significantly increased in HCC cells, and ligand-induced phosphorylation promoted HCC cell proliferation and migration and inhibited apoptosis. Additional studies revealed that the activation of IGF-1R phosphorylation promotes epithelial-mesenchymal transition in HCC cells by increasing the phosphorylation levels of Akt and GSK-3β. Collectively, our study findings suggest that IGF-1/IGF-1R promotes HCC progression by activating the Akt/GSK-3β pathway.
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Registered trials
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