fig4

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

Figure 4. Oncogenic Mutations and Glucose Metabolic Dysregulation in CCA: Therapeutic Targets and Metabolic Shifts. This figure illustrates the upregulation of key glycolytic enzymes (highlighted in red) and the associated metabolites involved in the metabolic alterations observed in cholangiocarcinoma. Additionally, it depicts common oncogenic mutations that modulate glucose metabolic reprogramming in CCA. The dotted arrows represent the regulation of glycolytic enzyme alterations and glucose metabolism dysregulation driven by common oncogenic mutations in CCA. Therapeutic targets are indicated adjacent to each corresponding oncogenic mutation to highlight potential intervention points. Created in BioRender. Chanda M. (2025) https://BioRender.com/3fv47uu. CCA: Cholangiocarcinoma; GLUT1: glucose transporter 1; HKII: hexokinase II; PFK1: phosphofructokinase-1; ALDOA: aldolase A; PKM2: pyruvate kinase M2; G6PD: glucose-6-phosphate dehydrogenase; 6PGD: 6-phosphogluconate dehydrogenase; TKT: transketolase; TALDO: transaldolase; LDHA: lactate dehydrogenase A; PDH: pyruvate dehydrogenase; TCA: tricarboxylic acid cycle; ICT: isocitrate; α-KG: alpha-ketoglutarate; OXPHOS: oxidative phosphorylation; KRAS: Kirsten rat sarcoma viral oncogene homolog; TP53: tumor protein p53; IDH: isocitrate dehydrogenase; ARID1A: AT-rich interaction domain 1A; FGFR2: fibroblast growth factor receptor 2; HER2: human epidermal growth factor receptor 2; GLUTs: other glucose tanspoters; ATP: adenosine triphosphate; ADP: adenosine diphosphate; Pi: inorganic phosphate.

Hepatoma Research
ISSN 2454-2520 (Online) 2394-5079 (Print)

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