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. 2023 Feb 10;9:56. doi: 10.1038/s41420-023-01355-8

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© The Author(s) 2023

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 1 — A TCGA STAD dataset analysis showed that the expression of NAT10 in HCC patients was significantly higher than that in healthy people (P < 0.0001). B GEO database (GSE 7186) was used to evaluate the expression of NAT10 in HCC tissues and corresponding adjacent tissues (n = 50), and the expression of NAT10 in cancer tissues significantly upregulated P < 0.001). C Kaplan–Meier analysis showed that the OS, PPS, and DSS of HCC patients with high NAT10 expression were significantly lower than those with low NAT10 expression. D qRT-PCR showed that the expression levels of Huh-7 and Hep3B NAT10 in four HCC cell lines were significantly upregulated compared with those in normal hepatocytes LO2. E Protein analysis of NTA10 in LO2 and different HCC cell lines by Western blot showed significant expression of NAT10 protein in Hep3b and Huh-7. Each experiment was performed in triplicate, and data are shown as mean ± standard deviation. *P < 0.05, **P < 0.01, ***P < 0.001.