ArticleCell death and differentiation2021
The noncoding RNAs SNORD50A and SNORD50B-mediated TRIM21-GMPS interaction promotes the growth of p53 wild-type breast cancers by degrading p53.
Article in Cell death and differentiation, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers, 1 of them a synthesis that pooled it.
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Who cites it
47 citing papers in PubMed, 1 synthesis or guideline pooled it, 56 citations in OpenAlex.
- Small Nucleolar RNAs as Diagnostic and Prognostic Biomarkers in Cancer: A Systematic Review and Meta-Analysis.Technology in cancer research & treatmentPooled it
- Disrupting KRAS-AGO2 interaction: a dual-pronged strategy to sensitize chemo-immunotherapy in KRAS-mutated colorectal cancer.Apoptosis : an international journal on programmed cell death · 2026Article
- snoRNAs and their derived sdRNAs: Emerging regulators, biomarkers, and therapeutic targets in human cancers (Review).International journal of oncology · 2026Review
- SnoRNA and SNHG in Bladder Cancer: Molecular Mechanisms and Clinical Significance.Current issues in molecular biology · 2026Review
- SNORD50A/B disassemble ASC-1 complex to silence NF-κB and boost PD-1 blockade in non-small-cell lung cancer.NPJ precision oncology · 2026Article
- RNA-binding proteins and ribonucleoproteins as determinants of immunity.Nature reviews. Immunology · 2026Review
- Downregulation of GMPS inhibited the proliferation of hepatocellular cancer cellsEuropean journal of histochemistry : EJH · 2026Article
- Review
- Hepatitis virus-associated B cell non-Hodgkin's lymphoma involves dysregulated epigenetic and RNA-mediated regulatory gene expression and altered snoRNA transcription.Scientific reports · 2026Article
- 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
- Non-coding RNAs as regulators of chromosomal instability in breast cancer.Frontiers in oncology · 2026Review
- Review
- Function and Mechanism of Small Nucleolar RNAs (snoRNAs) and Their Host Genes (SNHGs) in Malignant Tumors.Biomolecules · 2025Review
- Identification of potential blood biomarkers of coronary artery disease using a cuproptosis gene set.European journal of medical research · 2025Article
- KDM1A-driven RNF81 downregulation promotes gastric cancer progression via KLF4 destabilization.Oncogene · 2025Article
- Epigenetic Modulation and Bone Metastasis: Evolving Therapeutic Strategies.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Small Nucleolar RNAs: Biological Functions and Diseases.MedComm · 2025Review
- PAICS-Driven Purine Biosynthesis and Its Prognostic Implications in Lung Adenocarcinoma: A Novel Risk Stratification Model and Therapeutic Insights.Current issues in molecular biology · 2025Article
- A STT3A-dependent PD-L1 glycosylation modification mediated by GMPS drives tumor immune evasion in hepatocellular carcinoma.Cell death and differentiation · 2025Article
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Authors and funding
11 authors at 1 institution in 1 country.
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Abstract
Small nucleolar RNA SNORD50A and SNORD50B (SNORD50A/B) has been reported to be recurrently deleted and function as a putative tumor suppressor in different types of cancer by binding to and suppressing the activity of the KRAS oncoproteins. Its deletion correlates with poorer patient survival. However, in this study, we surprisingly found that SNORD50A/B loss predicted a better survival in breast cancer patients carrying wild-type p53. Functional studies showed that SNORD50A/B deletion strongly inhibited the proliferation, migration, invasion and tumorigenic potential, and induced cell cycle arrest and apoptosis in p53 wild-type breast cancer cells, while exerted the opposite effects in p53 mutated breast cancer cells. This was also supported by ectopically expressing SNORD50A/B in both p53 wild-type and mutated breast cancer cells. Mechanistically, SNORD50A/B clearly enhances the interaction between E3 ubiquitin ligase TRIM21 and its substrate GMPS by forming a complex among them, thereby promoting GMPS ubiquitination and its subsequent cytoplasmic sequestration. SNORD50A/B deletion in p53 wild-type breast cancer cells will release GMPS and induce the translocation of GMPS into the nucleus, where GMPS can recruit USP7 and form a complex with p53, thereby decreasing p53 ubiquitination, stabilizing p53 proteins, and inhibiting malignant phenotypes of cancer cells. Altogether, the present study first reports that SNORD50A/B plays an oncogenic role in p53 wild-type breast cancers by mediating TRIM21-GMPS interaction.
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