Fig 2: Association between NAT10 expression levels and patient prognosis based on multiple tumors from TCGA database. (A) Relationship of NAT10 expression with OS. (B) Relationship of NAT10 expression with progression-free interval (PFI). (C) Relationship of NAT10 expression with disease-free interval (DFI). (D) Relationship of NAT10 expression with DSS. Cox regression analysis; P < 0.05 was considered significant.

Fig 3: Transcripts modulated by NAT10-mediated ac4C modification in oocytes. (A) Venn diagram and pie chart showed the proportion of NAT10-regulated ac4C genes and non–ac4C-modified genes. (B) Box diagram displayed the fold change difference between NAT10-regulated ac4C-modified DEGs and non–ac4C-modified DEGs. (C) Sixteen downregulated ac4C-modified DEGs regulated by NAT10 mainly participated in regulation of protein binding and positive regulation of transcription, DNA-templated. (D) KEGG analysis showed 16 downregulated ac4C-modified DEGs regulated by NAT10 were enriched in cancer, signal transduction, folding, sorting, and degradation. Unpaired t-test was used in (B) to compare the expression of genes because the number of genes did not match between two groups. **P < 0.01.

Fig 4: NAT10 acetylates BCL-XL mRNA to enhance its translation efficiency and activates PI3K-AKT pathway to induce anti-apoptosis in MM cells. (A) WB examined the expressions of BCL-XL, AKT and p-AKT in OPM2 and KMS28-PE cells. (B) WB detected the expressions of BCL-XL and BAX in OPM2 and KMS28-PE cells. (C) WB tested the expressions of caspase-3 & cleaved caspase-3 and PARP & cleaved PARP in OPM2 and KMS28-PE cells.

Fig 5: NAT10 acetylates mRNA to regulate the progression of MM. (A) Schematic of acRIP-seq. (B) GO analysis of acRIP-seq. (C) Dot bolt showed that NAT10 overexpression led to higher mRNA acetylation level, and converse result was observed in siNAT10 MM cells.