ArticleMolecular and cellular biochemistry2026
The oncogenic role of NSUN2 in lung adenocarcinoma by stabilizing CCT5 mRNA via a YBX1-dependent m5C modification.
Article in Molecular and cellular biochemistry, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- The deubiquitinase USP5 mediates anti-PD-L1 resistance in breast cancer by stabilizing FOXM1 to upregulate Nectin2.Human cell · 2026Article
- RNA-Binding Peptide Influences Epitranscriptomic Regulation by Preferentially Binding to Unmodified RNAs Targeted by NSUN2.Biomolecules · 2026Article
- The role of FOXM1 in tumor immunology: implications for cancer treatment strategies.Human cell · 2026Review
- YBX1 as an adaptive RNA hub in cancer: linking state-dependent RNA regulation to tumor immunity, metabolic reprogramming, and therapy resistance.Frontiers in immunology · 2026Review
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Authors and funding
3 authors.
Funding
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Abstract
5-methylcytosine (m5C) methylation is a post-transcriptional modification of RNAs, and its dysregulation plays pro-tumorigenic roles in lung adenocarcinoma (LUAD). Here, this study elucidated the mechanism of action of NSUN2, a major m5C methyltransferase, on LUAD progression. mRNA expression was analyzed by quantitative PCR. Protein expression was tested by immunohistochemistry and immunoblotting. Cell proliferation was evaluated by MTT and EdU assays. Cell apoptosis was detected by flow cytometry and TUNEL staining. Transwell assays were used to examine cell invasion and migration. The influence of NSUN2 or the m5C reader YBX1 in CCT5 mRNA was analyzed by RNA immunoprecipitation assay and Actinomycin D treatment. In human LUAD, NSUN2 expression was upregulated, and high NSUN2 expression foreboded worse overall survival of LUAD patients. NSUN2 knockdown suppressed cell proliferation, diminished invasive and migratory potentials, and stimulated apoptosis in LUAD cells. NSUN2 was positively associated with CCT5 expression in LUAD and could mediate m5C modification of CCT5 mRNA. NSUN2 enhanced CCT5 mRNA stability and protein expression via two specific cysteines (C271 and C321). Moreover, YBX1 promoted CCT5 mRNA stability and protein expression. Additionally, restoration of CCT5 expression abolished NSUN2 deletion-mediated in vitro anti-proliferation, pro-apoptosis, anti-migration, and anti-invasiveness effects in LUAD cells, as well as in vivo anti-tumor growth behavior. Our study indicates that NSUN2 enhances the stability of CCT5 mRNA through a YBX1-m5C-dependent manner to drive LUAD progression. Targeting the NSUN2/CCT5 axis may be a potential approach to combat LUAD.
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Registered trials
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