Fig. 3: PFKFB3 inhibition led to G2/M phase arrest and apoptosis of HCC cells.
From: PFKFB3 blockade inhibits hepatocellular carcinoma growth by impairing DNA repair through AKT
a Glucose consumption of different PFKFB3 expressions of SMMC7721 and Huh7 cells. High expression cells consumoted more glucose. b Immunofluorescence stain of PFKFB3 in SMMC7721 and Huh7 cells. PFKFB3 located both in nucleus and cytoplasm. c Clone formation of SMMC7721-shPFKFB3 cells and Huh7-PFKFB3 cells compared with their vector control in glucose substitute medium. PFKFB3 promoted the cells clone formation eliminating the effect of glucose in vitro. d CCK8 assay for cell proliferation of SMMC7721-shPFKFB3 cells and Huh7-PFKFB3 cells compared with their vector control in glucose substitute medium. PFKFB3 promoted the liver cancer cells proliferation eliminating the effect of glucose in vitro. e Flow cell apoptosis detection for cell apoptosis rates of SMMC7721-shPFKFB3 cells and Huh7-PFKFB3 cells compared with their vector control in glucose substitute medium. PFKFB3 decreased the apoptosis rate of liver cancer cells eliminating the effect of glucose in vitro. f Flow cytometry cycle detection of the cell cycle ratio of SMMC7721-shPFKFB3 cells and Huh7-PFKFB3 cells compared with their vector control in glucose substitute medium. PFKFB3 knockdown increased the proportion of G2/M phase. **p < 0.01
