ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025
SNORA74A Drives Self-Renewal of Liver Cancer Stem Cells and Hepatocarcinogenesis Through Activation of Notch3 Signaling.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- Crosstalk between alternative splicing and non-coding RNAs in hepatocellular carcinoma: from regulatory mechanism to therapeutic implications.Non-coding RNA research · 2026Review
- Article
- snoRNAs and their derived sdRNAs: Emerging regulators, biomarkers, and therapeutic targets in human cancers (Review).International journal of oncology · 2026Review
- NF-κB signaling in hepatocellular carcinoma: Mechanisms of tumor progression, immune evasion, and therapeutic resistance.Translational oncology · 2026Review
- BUB1 promotes cell stem-like properties and serves as a diagnostic biomarker for lung cancer.Scientific reports · 2026Article
- NRAV promotes HCC stemness via the m6A-regulated let-7c-5p/LIN28B axis.Cancer gene therapy · 2026Article
- The dual role of the Notch signaling pathway in digestive system cancers.European journal of medical research · 2026Review
- Small Nucleolar RNAs (snoRNAs) in Cancer: From Biogenesis to Clinical Potential.OncoTargets and therapy · 2026Review
- Integrative analysis of a novel snoRNA-based prognostic signature in patients with breast cancer.Frontiers in oncology · 2026Article
- H/ACA snoRNAs and snoRNPs Dysregulation Links rRNA Modification to Glioblastoma Progression.Research square · 2025Article
- SNORA74A Drives Self-Renewal of Liver Cancer Stem Cells and Hepatocarcinogenesis Through Activation of Notch3 Signaling.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
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Authors and funding
13 authors.
Funding
Abstract
Liver cancer stem cells (CSCs) account for tumor initiation, heterogeneity and therapy resistance. However, the role of small nucleolar RNAs (snoRNAs) in the regulation of liver CSCs remains largely unclear. Here, this work identifies a conserved H/ACA box snoRNA SNORA74A which is highly expressed in liver CSCs. SNORA74A deletion impaired the self-renewal of liver CSCs and suppressed hepatocarcinogenesis. Mechanistically, highly expressed SNORA74A in liver CSCs bound DCAF13 to prevent K48 linked ubiquitination of E2F2 for degradation. E2F2 induced NOTCH3 transcription to initiate Notch3 signaling activation, leading to self-renewal of liver CSCs and hepatocarcinogenesis. Moreover, expression levels of SNORA74A and NOTCH3 are positively related with severity and poor prognosis of hepatocellular carcinoma (HCC) patients. Of note, antisense oligonucleotides (ASOs) against SNORA74A showed effective efficacy for HCC tumors, suggesting SNORA74A might be a potential therapeutic target for HCC therapy by eliminating liver CSCs.
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