IADR Abstract Archives
Nitric oxide modulates glycolysis in head and neck cancer cells
Objectives: Glycolysis is a crucial energy-providing process that represents one of the hallmarks of cancer. Nitric oxide (NO), a free radical molecule, has been reported to regulate glycolysis in various cancers. It has been observed that NO can alter the cell cycle and apoptosis in head and neck squamous cell carcinoma (HNSCC) cells. However, the precise effect of NO on glycolysis in HNSCC cells remains elusive. This study aimed to investigate the effects of NO on cell proliferation, gene expression of glucose transporters (GLUTs), and glycolytic indicators in HNSCC cell lines.
Methods: Two pairs of isogenic HNSCC cell lines, HN18/HN17 and HN30/HN31, were treated with a NO donor, DEA-NONOate, for 24, 48, and 72 hours. Cell proliferation was assessed using the MTT assay, and NO concentration was measured using the Griess Reagent System. Gene expressions of GLUT1, GLUT2, GLUT3, and GLUT4 were analyzed using real-time PCR. Additionally, hexokinase activity and lactate production were measured in NO-treated cells using colorimetric assays.
Results: The results revealed that DEA-NONOate concentrations of 0.5, 0.5, 10, and 100 µM significantly increased cell proliferation in HN18, HN17, HN30, and HN31 cells, respectively, at different time points. DEA-NONOate induced NO generation in a time-dependent manner in HN18, HN30, and HN31 cells, while no such effect was observed in HN17 cells. Interestingly, GLUT1 expression was differentially up-regulated in NO-treated HN18 cells compared to the control group. Furthermore, NO enhanced hexokinase activity and increased lactate production in HN18 cells.
Conclusions: In conclusion, this study demonstrated distinct proliferative effects of NO on HNSCC cells. Notably, NO treatment resulted in increased expression of glycolytic indicators, including GLUT1, hexokinase activity, and lactate production, in HN18 cells. These findings suggest that NO may promote cell proliferation by stimulating glucose consumption and glycolytic rate in HN18 cells.
Methods: Two pairs of isogenic HNSCC cell lines, HN18/HN17 and HN30/HN31, were treated with a NO donor, DEA-NONOate, for 24, 48, and 72 hours. Cell proliferation was assessed using the MTT assay, and NO concentration was measured using the Griess Reagent System. Gene expressions of GLUT1, GLUT2, GLUT3, and GLUT4 were analyzed using real-time PCR. Additionally, hexokinase activity and lactate production were measured in NO-treated cells using colorimetric assays.
Results: The results revealed that DEA-NONOate concentrations of 0.5, 0.5, 10, and 100 µM significantly increased cell proliferation in HN18, HN17, HN30, and HN31 cells, respectively, at different time points. DEA-NONOate induced NO generation in a time-dependent manner in HN18, HN30, and HN31 cells, while no such effect was observed in HN17 cells. Interestingly, GLUT1 expression was differentially up-regulated in NO-treated HN18 cells compared to the control group. Furthermore, NO enhanced hexokinase activity and increased lactate production in HN18 cells.
Conclusions: In conclusion, this study demonstrated distinct proliferative effects of NO on HNSCC cells. Notably, NO treatment resulted in increased expression of glycolytic indicators, including GLUT1, hexokinase activity, and lactate production, in HN18 cells. These findings suggest that NO may promote cell proliferation by stimulating glucose consumption and glycolytic rate in HN18 cells.