ArticleCellular & molecular biology letters2026
The NAT10/c-Myc positive feedback loop orchestrates tRNA ac
Article in Cellular & molecular biology letters, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundEpitranscriptomic regulation of tRNA modifications has emerged as an important mechanism in cancer progression by influencing oncogenic translation. Anaplastic thyroid carcinoma (ATC) is a highly aggressive malignancy with limited therapeutic options. Although N-acetyltransferase 10 (NAT10) is frequently overexpressed in multiple cancers, its functional role and therapeutic potential in ATC remain unclear.
methodsWe employed integrated approaches including bioinformatics analyses,in vitro and in vivo assays, multi-omics profiling (mRNA-seq, Ribo-seq, tRNA RedaC-seq), and mechanistic studies (ChIP, LC-MS and ubiquitination assays) in ATC cell lines and xenograft models.
resultsNAT10 is significantly upregulated in ATC and correlates with poor prognosis. Functional assay demonstrates that NAT10 enhances ATC cell proliferation and invasion in vitro and in vivo. The targeted inhibition of NAT10 using the small molecule inhibitor remodelin effectively suppresses ATC cell growth. Mechanistically, NAT10 forms a positive feedback loop with the transcription factor c-Myc: c-Myc transcriptionally activates NAT10, whereas NAT10 is associated with enhanced translation of c-Myc in conjunction with tRNA ac
conclusionsThese findings identify a NAT10/c-Myc positive feedback loop associated with tRNA ac
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