Fig. 1

NAT10 promotes gastric cancer progression through mRNA ac4C modification. a Graphical summary of this article. b The chemical structure of ac4C. c The expression of NAT10 in the TCGA STAD dataset. d High NAT10 expression was significantly associated with a shorter OS. e The ac4C significant consensus sequence motif was identified based on the acRIP-seq and RIP-seq analyses, and the significant consensus sequence of NAT10 bound and interacted. f KEGG pathway enrichment analysis and acRIP-seq analysis identified the enriched pathway of ac4C modification down-regulated genes after NAT10 silencing. g Overlapping the potential target bound and interacted with NAT10 in focal adhesion and ECM-receptor interaction pathway by the acRIP-seq and RIP-seq analysis. h Attenuation of the NAT10 diminishes the ac4C modification genome of COL5A1 mRNA visual result compared using the acRIP-seq (colored in deep blue). The visual genome result of COL5A1 mRNA bound and interacted with NAT10 (colored in wathet blue). i The regulatory role of NAT10 on COL5A1 ac4C in SGC-7901 and MGC-803 cells confirmed by the acRIP-qPCR assay. j The bound and interacted relationship between NAT10 and COL5A1 mRNA in SGC-7901 and MGC-803 cells confirmed using the RIP-qPCR assay. k, l Western blotting and qRT-PCR analyses of COL5A1 in shNAT10 or NAT10 overexpressing MGC-803 and SGC-7901 cells. m Wild-type (WT) or mutant COL5A1 cells were transfected with pmirGLO-COL5A1 reporter, respectively. n The transcriptional level of wild-type COL5A1, but not the mutation, significantly decreased in the NAT10-knockdown cells, and significantly increased in the NAT10 overexpressing cells. o The impression of NAT10 on COL5A1 mRNA stability confirmed by the RNA decay assay. p The impression of NAT10 on COL5A1 mRNA translation efficiency confirmed