Objective: This project investigated the inhibitory effect of Fraxetin on endometrial cancer cell proliferation, and explored the possibility of applying Fraxetin in the treatment of endometrial cancer.
Methods: Human endometrial cancer RL95-2 cell line was cultured in vitro, and the cells were administered different concentrations of Fraxetin. MTS was used to detect the inhibitory effect of Fraxetin on proliferation. Flow cytometry was applied to detect the effect of Fraxetin on RL95-2 cell cycle. Western blot was employed to determine the expression of apoptosis-related proteins, such as caspase-3, caspase-9, p-AMPK, AMPK, p-mTOR, and mTOR. JC-1 staining was used to measure the mitochondrial membrane potential changes in the cells before and after the administration. The glucose oxidase method and the lactate oxidase method were used to detect changes in glucose consumption and lactic acid production in endometrial cancer cells before and after drug intervention, respectively.
Results: Fraxetin inhibited cell proliferation and promoted apoptosis. The expressions of caspase-3 and caspase-9 increased significantly, p-AMPK gradually increased, and mitochondrial membrane potential weakened. Glucose consumption and lactic acid production increased significantly.
Conclusion: Fraxetin can inhibit the proliferation of RL95-2 cells, promote apoptosis, inhibit mitochondrial oxidation of endometrial cancer cells, promote anaerobic metabolism of cells, and exert an inhibitory effect on endometrial cancer cells by inhibiting mitochondria.
Keywords: Fraxetin; RL95-2 cells; apoptosis; mitochondria.
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