ArticleTranslational oncology2026
An ac4C-CDK4 regulatory axis driven by NAT10 sustains proliferative signaling in colorectal cancer.
Article in Translational oncology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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8 authors.
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Abstract
backgroundN-acetyltransferase 10 (NAT10) is an RNA acetyltransferase that catalyzes N4-acetylcytidine (ac⁴C) modification and regulates mRNA stability. However, its biological function and mechanistic role in colorectal cancer (CRC) remain poorly defined.
methodsNAT10 expression was analyzed across multiple GEO cohorts and paired CRC clinical specimens. Gain- and loss-of-function experiments were performed to assess the effects of NAT10 on CRC cell proliferation, migration, colony formation, and tumor growth in vivo. Transcriptomic correlation and enrichment analyses were used to identify NAT10-associated pathways. RIP-seq mining, NAT10-RIP-qPCR, and ac⁴C-RIP-qPCR were applied to verify downstream targets. Actinomycin D chase assays were used to evaluate mRNA stability. The functional relevance of CDK4 was examined using genetic NAT10 perturbation, Remodelin-based pharmacologic treatment, and CDK4 rescue experiments.
resultsNAT10 was markedly up-regulated in CRC tissues compared with normal mucosa and was maintained at high levels in malignant CRC lesions. NAT10 overexpression enhanced CRC cell proliferation, migration, and colony formation, whereas NAT10 knockout suppressed these phenotypes. In vivo, NAT10-deficient cells formed significantly smaller and slower-growing xenograft tumors, with markedly reduced tumor volume and weight compared with controls. Pathway analyses indicated strong enrichment of cell-cycle programs, particularly the G1/S transition. CDK4 was identified as a NAT10-associated ac⁴C-modified target. NAT10 depletion destabilized CDK4 mRNA, reduced CDK4-associated cell-cycle protein expression, and induced G1/S accumulation, while NAT10 overexpression produced the opposite effects. Remodelin treatment, used as a pharmacologic perturbation of NAT10-associated signaling, suppressed CDK4 expression and CRC cell growth, and CDK4 overexpression partially rescued these inhibitory effects.
conclusionsThis study identifies a mechanistic NAT10-ac⁴C-CDK4 regulatory axis that stabilizes CDK4 mRNA, promotes G1/S transition, and drives CRC progression. Targeting NAT10 or its downstream CDK4 pathway represents a potential therapeutic strategy for CRC.
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