Study on the mechanism of bezafibrate inhibiting glycolysis in lung adenocarcinoma through AKT/mTOR pathway
Objective To study the inhibitory effect and mechanism of bezafibrate on the growth of lung adenocarcinoma A549 cells.Methods Logarithmic growth stage A549 cells were selected and divided into bezafibrate groups(25,50,100,200,400 µmol/L),negative control group,and blank control group.After 48 and 72 hours of drug intervention,the inhibition rate of A549 cell proliferation was detected by CCK-8 method.The contents of glucose and lactic acid in cell medium of each group were determined,the glucose consumption rate and lactic acid production were calculated,and the effects of different concentrations of bezafibrate on aerobic glycolysis of A549 cells were evaluated.The expression of Akt,mTOR and PKM2 protein in high,medium and low concentrations of bezafibrate groups were detected by western blot.Results Bezafibrate significantly inhibited the proliferation of lung adenocarcinoma A549 cells,and the inhibitory effect was proportional to the drug concentration.Bezafibrate affected the glycolysis process of A549 cells.With the increase of drug concentration,glucose consumption and lactic acid production in cells decreased.Bezafibrate inhibited the expression of Ak,mTOR and PKM2 protein in a concentration-dependent manner.Conclusion Bezafibrate can promote apoptosis of lung adenocarcinoma A549 cells,which may be related to inhibition of glycolysis pathway and reversal of warburg effect in tumor cells.
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