1, 25-dihydroxyvitamin D3 promotes apoptosis in human breast cancer MCF-7 cells by glycolysis pathway
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Abstract:
Objective: To investigate the effect of 1, 25-dihydroxyvitamin D3 (VD3) on apoptosis of human breast cancer MCF-7 cells and its mechanism. Methods: Human breast cancer MCF-7 cells cultured in vitro were randomly divided into 6 groups: control group, 2-DG group, 1 μmol/L VD3 group, 10 μmol/L VD3 group, 2-DG+1 μmol/L VD3 group and 2-DG+10 μmol/L VD3 group. The cells in 6 groups were detected 48 h after they were treated with VD3 or 2-DG. The glucose uptake assay was used to measure the glucose uptake of cells, the ATP content in the cells was measured by the ATP kit, and the lactate level was measured by the lactate kit. The expression levels of cytochrome C (Cyt c) and apoptosis-associated proteins (Bcl-2, BAX, PARP1, caspase9 and caspase3) in MCF-7 cells were detected by WB method. Results: Compared with the control group, after the intervention of VD3, the apoptosis rate of MCF-7 cells increased significantly (P<0.05 or P<0.01), the glucose uptake, ATP content and lactate level were significantly decreased (P<0.05 or P<0.01), the expression of Cyt c, BAX, PARP1, caspase9 and caspase3 protein was significantly increased (all P<0.05), and the expression of Bcl-2 protein was decreased (P<0.05 or P<0.01); after the intervention of VD3 combined with 2-DG, the changes in the detection indexes of each group were more obvious (P<0.05 or P<0.01). Conclusion: VD3 can inhibit glycolysis of human breast cancer MCF-7 cells and induce apoptosis through the mitochondrial Cyt c pathway.