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Apigenin Inhibits Glycolysis and Spheroid Formation via Downregulation of HK-2 Expression in Non-Small Cell Lung Cancer H460 Cells |
SUN Fei, YUAN Qing, ZHANG Jiansong |
School of Medicine, Hunan Normal University, Changsha 410013, China |
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Abstract Objective To investigate whether apigenin (API) inhibits the glycolysis and self-renewal capacity by downregulating the expression of glucose metabolism related kinase HK-2 in non-small cell lung cancer (NSCLC) H460 cells in vitro. Methods H460 cells were transfected with HK-2 cDNA, treated with sub-cytotoxicity concentrations of API (20 μM; 40 μM and 80 μM) or in combination with API (80 μM) treatment and HK-2 cDNA transfection. Western blot was utilized to detect the expression of HK-2. The levels of lactate production and glucose consumption were using measurement of lactate production and glucose consumption assays. The spheroid formation assay was employed to detect the self-renewal capacity in H460 cells. Results The sub-cytotoxic concentrations of API decreased the expression of glucose metabolism related kinase HK-2 and reduced lactiate production and glucose consumption, as well as decreased sphere formation rate in NSCLC H460 cells in a dose-dependent tendency. Moreover, overexpression of HK-2 could rescue the inhibitory effects of API on lactate production, glucose consumption and spheroid formation in NSCLC H460 cells. Conclusion API can inhibit glycolysis and self-renewal capacity by downregulating HK-2 expression in NSCLC H460 cells.
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Received: 15 December 2022
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