fig3

Figure 3. Potential CCA therapeutic targets based on glucose metabolism. Upregulation of genes involving glycolysis in CCA provides opportunities to develop targeted therapies. Previous reports showed that inhibiting the expression of GLUT1, GLUT5, and HK2 by siRNA, and LDHA by metformin combined with BG-45, significantly reduced CCA cell proliferation and induced cell apoptosis. Additionally, inhibition of the activities of GLUT1, HK2, and PKM2 by their inhibitor also retarded CCA cell growth. Glc: Glucose; G-6-P: glucose-6-phosphate, F-6-P: fructose-6-phosphate; PEP: phosphoenolpyruvate; CCA: cholangiocarcinoma; GLUT1: glucose transporters 1; GLUT5: glucose transporter 5; HK2: hexokinase II; LDHA: lactate dehydrogenase A; PKM2: pyruvate kinase isoform M2.