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Fig. 5 | Journal of Translational Medicine

Fig. 5

From: Histidine metabolism drives liver cancer progression via immune microenvironment modulation through metabolic reprogramming

Fig. 5

Construction of a Prognostic Model for Hepatocellular Carcinoma Based on High Histidine Metabolism. (A) Forest plot displaying the association between histidine metabolism-related genes and the survival of liver cancer patients. (B) Kaplan-Meier survival curves for patients with histidine metabolism-related gene expression, analyzed using TCGA data. (C) Construction of a lasso prognostic model using histidine metabolism-related genes. (D) Venn diagram displaying genes included in both the lasso prognostic model and those associated with the survival of liver cancer patients. (E) TCGA data analysis of BUD23 gene expression and its association with tumor status, pathological T stage, pathological stage, and histological grade in liver cancer patients. (F) Correlation of BUD23 expression with infiltration of various immune cell types in TCGA data. (G) Correlation of AOC1 expression with infiltration of various immune cell types in TCGA data. (H) Seahorse analysis of the impact of BUD23 and AOC1 expression on oxygen consumption rate (OCR). (I) Seahorse analysis of the impact of BUD23 and AOC1 expression on glycolytic rate (glycoPER). (K) Flow cytometry assessing the effects of BUD23 or AOC1 knockdown on T-cells differentiation: CD3⁺CD4⁺ T cells (upper), CD3⁺CD8⁺ T cells (lower). (L) Flow cytometry assessing the effects of BUD23 or AOC1 knockdown on T-cells function: CD69 expression (upper), PD-1 expression (lower). (L) Flow cytometry examining macrophage polarization following BUD23 or AOC1 knockdown. Error bars represent the SD of three or five independent experiments, ns, not significant, ***P < 0.001

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