ArticleCell death & disease2025
Nucleolar NOL9 regulated by DNA methylation promotes hepatocellular carcinoma growth through activation of Wnt/β-catenin signaling pathway.
Article in Cell death & disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Integrative single-cell and machine learning analysis identifies a tumor doubling time-related prognostic signature and therapeutic targets in head and neck squamous cell carcinoma.Translational oncology · 2026Article
- Integrative single-cell and spatial transcriptomics analysis reveals a baicalein-responsive 10-gene signature for non-small cell lung cancer.Translational oncology · 2026Article
- Multi-omics integration identifies ribosome biogenesis-active macrophage subpopulation and its key gene GNL2 in driving liver hepatocellular carcinoma progression and mechanisms.Cancer cell international · 2026Article
- Novel Therapeutics for Hepatocellular Carcinoma.Clinics in liver disease · 2025Review
- Targeting immune checkpoints in hepatocellular carcinoma therapy: toward combination strategies with curative potential.Experimental hematology & oncology · 2025Review
- Lactylation-related gene signatures identify glioma molecular subtypes with prognostic, immunological, and therapeutic implications.Frontiers in oncology · 2025Article
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Authors and funding
12 authors.
Funding
Abstract
Ribosome biogenesis (RiboSis) and ribosomal stress are critical in tumor progression, positioning RiboSis as a promising therapeutic target for cancer treatment and for overcoming drug resistance. In this study, we examined the role of RiboSis in the progression from hepatitis B virus (HBV) infection to HBV-related hepatocellular carcinoma (HCC), focusing specifically on nucleolar protein 9 (NOL9) and its influence on HCC pathogenesis and therapeutic response. Our findings showed that NOL9 was significantly upregulated in HCC tissues, correlating with larger tumor sizes and more advanced pathological grades. High levels of NOL9 expression were associated with unfavorable prognosis in both the TCGA-LIHC and our HCC cohorts. Functional assays indicated that NOL9 regulated HCC cell proliferation and apoptosis; specifically, NOL9 knockdown inhibited cell proliferation and promoted apoptosis, while overexpression enhanced these processes. In vivo studies confirmed that NOL9 depletion reduced tumor growth. Mechanistically, NOL9 expression was regulated by DNA methylation and the transcription factor ZNF384. Our DNA methylation analysis revealed an inverse correlation between NOL9 expression and methylation at specific CpG sites, implicating DNMT1 in its epigenetic regulation. Additionally, NOL9-mediated cell proliferation was dependent on activation of the Wnt/β-catenin signaling pathway. This study highlights the multifaceted role of NOL9 in HCC pathogenesis, underscoring its potential as a diagnostic biomarker and therapeutic target.
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