ArticleJournal of cancer research and clinical oncology2025
NSUN5 promotes cholangiocarcinoma progression by enhancing GLS mRNA stabilization.
Article in Journal of cancer research and clinical oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Oxidative stress-driven mRedox biology · 2026Article
- RNA methylation in cell death: mechanisms and clinical applications.Molecular cancer · 2026Review
- mBiology direct · 2026Review
- RNA Regulatory Networks: Key Hubs in the Panorama of Cancer and Emerging Therapeutic Targets.MedComm · 2026Review
- NSUN5 and RNA mFrontiers in cell and developmental biology · 2026Review
- NSUNs-driven dysregulation: the next frontier in targeted cancer therapy?Cell death & disease · 2025Review
- The Role of NSUN Family Genes in m5C Methylation and Diseases.Biomedicines · 2025Review
- Epitranscriptomic modifications in programmed cell death: mechanistic insights and implications for liver diseases.Cellular & molecular biology letters · 2025Review
- NSUN5 Mediates Resistance to Doxorubicin via Up-regulation of DNA Damage Repair Proteins BRCA2 and BRIP1 in Colorectal Cancer.The American journal of pathology · 2025Article
- Epitranscriptomic mechanisms and implications of RNA mTheranostics · 2025Review
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4 authors.
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Abstract
backgroundNSUN5, also known as NOP2/Sun domain 5, is a pivotal RNA methyltransferase that catalyzes the formation of 5-methylcytosine (m5C). Cuproptosis, induced by elevated copper concentrations, is under investigation as a potential therapeutic strategy for cancer treatment. Despite this, the specific roles and the molecular mechanisms underlying Cuproptosis and NSUN5-mediated m5C modification in cholangiocarcinoma (CCA) remain to be fully elucidated.
methodsHuman tissue samples were collected to assess the expression levels of NSUN5 in CCA. In vitro functional assays were conducted to evaluate the biological function of NSUN5. The functional mechanism of NSUN5 on glutaminase (GLS) was investigated using RNA pull-down, RNA immunoprecipitation, molecular docking, and RNA stability assays.
resultsThis study identified an upregulation of NSUN5 in CCA tissues. The knockdown of NSUN5 diminished the proliferation, migration, and invasion capabilities of CCA cells in vitro. In contrast, the overexpression of NSUN5 enhanced the growth and metastasis of CCA cells. Additionally, an increased copper content was detected in CCA tissues, which correlated with aggressive clinical features. CCA cells exhibited resistance to cuproptosis by upregulating GLS expression. Functionally, NSUN5 was found to positively modulate GLS expression. The NSUN5-mediated m5C modification at site 137 C on the GLS mRNA sequence stabilizes the GLS mRNA, leading to an accumulation of GLS within cells.
conclusionsOur findings highlight the critical role of NSUN5 in CCA progression through m5C-dependent stabilization of the GLS transcript, suggesting a potential targeted therapeutic strategy for CCA.
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