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. 2023 Feb 7;14(2):87. doi: 10.1038/s41419-023-05625-2

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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. 7 — a Relative protein levels of p53, ACOX1, KAT2B, ATIC. The results shown are from the same tissues shown in Fig. S7a. Signal intensity of these proteins were quantified by Image J, and then normalized to β-actin band intensity. b ACOX1, KAT2B, ATIC expression in CRC tumors and normal colorectal tissues. The raw data from TCGA. c Correlation between the expression levels of p53 and ACOX1, KAT2B, ATIC, as determined by Pearson’s r analysis. The results shown are from the same tissues shown in Fig. S7a. d Correlation between the expression levels of Ac-ATIC and p53, ACOX1, KAT2B, as determined by Pearson’s r analysis. The results shown are from the same tissues shown in Fig. S7a. e Kaplan–Meier analysis of overall survival (OS) in CRC patients according to the expression of peroxisomal FAO. P values were calculated by log-rank test. The raw data was from TCGA. f Schematic illustration of the mechanistic model for the role of p53-mediated peroxisomal β-oxidation-ATIC axis in colorectal tumorigenesis. Data were presented as mean ± SD.