Fig. 1

Expression profile of PARD3 during metabolic dysfunction-associated liver carcinogenesis. A. Diagram showing the process for establishment of the CDAA diet- and MCD diet-induced mouse hepatocarcinogenesis models. B&C. The relative mRNA expression level of PARD3 in mice with diet-induced liver cancer and their control diet-fed littermates. D&E. Expression of PARD3 was induced in the tumorigenesis stage rather than in metabolic liver disease stages. F. Transcriptional analysis of liver with or without surface tumours from C57BL/J mice after CDAA diet feeding for 54 weeks. G. GO enrichment analysis and heatmap of upregulated polarity-related genes in livers with tumour nodules compared with tumour-free livers. H. GSEA results showing that the establishment of cell polarity pathway was enriched in CDAA diet-fed mice with tumour nodule development. Upon PARD3 knockout, the hepatic I. tumour burden, J. tumour incidence, K. tumour number and L. tumour volume were significantly reduced in CDAA diet- and MCD diet-fed mice. PARD3 knockout significantly reduced the expression of M. AFP and decreased the N. Ki67⁺ cell population. *P < 0.05; **P < 0.01; ***P < 0.001; n.s., not statistically significant