fig3

From: Glucose metabolic dysregulation and oxidative stress in cholangiocarcinoma: molecular mechanisms, oncogenic drivers, and novel therapeutic targets

Glucose metabolic dysregulation and oxidative stress in cholangiocarcinoma: molecular mechanisms, oncogenic drivers, and novel therapeutic targets

Figure 3. Differential expression of glucose metabolic enzymes in CCA. The distribution of gene expression levels is displayed using box plots (red: tumor tissues; blue: normal tissues) in panels A-I. (A) HKII; (B) PFKP; (C) ALDOA; (D) PKM2; (E) G6PD; (F) 6PGD; (G) TKT; (H) TALDO; (I) LDHA. Statistical significance was determined using the Wilcoxon test, with P-values indicated by the number of stars (^*P-value < 0.05; ^**P-value < 0.01; ^***P-value < 0.001). Created using Timer2.0 and the TCGA database. CCA: Cholangiocarcinoma; HKII: hexokinase II; PFKP: phosphofructokinase platelet form; ALDOA: aldolase A; PKM2: pyruvate kinase M2; G6PD: glucose-6-phosphate dehydrogenase; 6PGD: 6-phosphogluconate dehydrogenase; TKT: transketolase; TALDO: transaldolase; LDHA: lactate dehydrogenase A.