ArticleCell & bioscience2026
ELYS promotes hepatocellular carcinoma stemness by activating a FOXO6-NUP205 transcriptional module downstream of PI3K/AKT to drive Hedgehog signaling.
Article in Cell & bioscience, 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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Abstract
backgroundHepatocellular carcinoma (HCC) is a lethal malignancy driven by cancer stem cells, which drive progression and therapeutic resistance. Nuclear pore protein ELYS is implicated in tumorigenesis, but its role in HCC stemness remains unclear.
methodsTranscriptome sequencing identified ELYS-induced differentially expressed genes (DEGs). Functional impacts of ELYS on malignant phenotypes and stemness were assessed in vitro. Signaling pathway activation was confirmed using inhibitors of Hedgehog (GANT-61) and AKT (MK-2206 2HCl). Bioinformatics analysis, luciferase reporter, and ChIP assays elucidated the FOXO6-NUP205 axis. Xenograft models validated the findings in vivo. Clinical relevance was evaluated using TCGA-HCC data and immunohistochemistry in clinical samples.
resultsDEGs in ELYS-overexpressing cells were enriched in PI3K/AKT and Hedgehog (Hh) pathways. ELYS facilitated Gli-1 nuclear translocation by activating PI3K/AKT, placing it upstream of Hh. Bioinformatic and experimental analyses identified FOXO6 and its target NUP205 as key effectors. ELYS upregulated FOXO6, which directly activated NUP205 transcription. FOXO6 knockdown suppressed ELYS-induced effects on NUP205, Gli-1 nuclear translocation, and stemness factors. In vivo, ELYS promoted tumor growth and lung metastasis via PI3K/AKT/Hh. Clinically, ELYS, FOXO6, and NUP205 were overexpressed in HCC, correlating with advanced features and poor survival.
conclusionThis study defines an oncogenic axis wherein ELYS promotes HCC stemness and metastasis by activating PI3K/AKT, triggering a FOXO6-NUP205 cascade to drive Hedgehog, representing a pivotal mechanism and therapeutic target.
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