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. 2021 Nov;9(22):1701. doi: 10.21037/atm-21-5975

Figure 4.

Figure 4

Andro suppresses NSCLC cell proliferation by inducing the reprogramming of glucose metabolism. (A) Andro reduced the expression of PKM2, LDHA, and GLUT1 genes, and stimulated the expression of PEPCK1, FBP1, and PFK genes in H1975 cells, as measured by qRT-PCR; (B) Andro inhibited glucose uptake, lactate production, and intracellular ATP synthesis in H1975 cells; (C) FBP1-siRNA significantly inhibited FBP1 expression at both the mRNA and protein levels in H1975 cells, as measured by qRT-PCR and WB; (D) in H1975 cells, FBP1 downregulation promoted glucose uptake, lactate production, intracellular ATP synthesis; (E) FBP1 downregulation promoted H1975 cell proliferation, as evaluated through the CCK-8 assay; (F) FBP1 downregulation inhibited cleaved caspase 9, cleaved caspase 8, and cleaved caspase 3 gene expression, as evaluated through WB. *, P<0.05; **, P<0.01. Andro, andrographolide; NSCLC, non-small cell lung cancer; PKM2, pyruvate kinase M2; LDHA, lactate dehydrogenase A; GLUT1, glucose transporter 1; PEPCK1, phosphoenolpyruvate carboxykinase 1; FBP1, fructose-1,6-bisphosphatase 1; PFK, phosphofructokinase; GAPDH, glyceraldehyde-3-phosphate dehydrogenase; ATP, adenosine triphosphate; qRT-PCR, real-time quantitative reverse transcription-polymerase chain reaction; Mrna, messenger RNA; WB, western blotting; CCK-8, cell counting kit-8; OD, optical density; NC, negative control; si, small interfering.