ArticleCytoJournal2026
SOX2 promotes the progression of hepatocellular carcinoma by targeting FOXJ3 and activating the PI3K/AKT pathway to regulate autophagy and mitophagy.
Article in CytoJournal, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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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.
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Abstract
Objectives: Sex-determining region Y-box transcription factor 2 ( SOX2) has been implicated in tumorigenesis across various cancers. This study sought to characterize the expression pattern of SOX2 in hepatocellular carcinoma (HCC) and elucidate its potential mechanism in promoting HCC progression by targeting Forkhead box J3 (FOXJ3) and regulating the phosphoinositide 3-kinase/protein kinase B (PI3K/AKT) signaling pathway, autophagy, and mitophagy. Material and Methods: SOX2 expression was examined in normal liver epithelial (THLE2) and HCC (Huh7) cells. It was modulated by shRNA-mediated knockdown and plasmid-based overexpression. 5-Ethynyl-2'-deoxyuridine (EdU) fluorescence staining assay, Transwell assays, and flow cytometry were performed to evaluate cell viability and motility. Autophagy and mitophagy were assessed by Western blotting and transmission electron microscopy, and mitochondria-lysosome co-localization was visualized by immunofluorescence staining. The roles of SOX2 and FOXJ3 in the PI3K/AKT signaling pathway were investigated. Results: SOX2 was markedly upregulated in HCC cells ( Conclusion: SOX2 promotes HCC progression by negatively regulating FOXJ3, thereby activating the PI3K/AKT signaling pathway and inducing autophagy and mitophagy. The potential SOX2-FOXJ3-PI3K/AKT axis may serve as a novel regulatory pathway underlying HCC development and represents a potential target for therapeutic intervention.
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