Found programs:
Authors:Yang Yali; Zhang Shengyuan; Pan Zengfeng
Keywords:nicotinamide;CNE-1 cells;proliferation;apoptosis;migration
DOI:10.19405/j.cnki.issn1000-1492.2021.03.016
〔Abstract〕 Objective To investigate the effect and potential mechanism of nicotinamide on proliferation, apoptosis and migration of nasopharyngeal carcinoma(NPC) CNE-1 cells. Methods NPC CNE-1 cells were divided into blank control group and the experimental groups, which were treated with 10, 20, 40 and 80 μmol/L of nicotinamide respectively, while the blank control was treated without nicotinamide. The proliferation rate of CNE-1 cells was detected by CCK-8 after 48 h and 72 h treatment with the concentrations mentioned above, the apoptosis rates and the cell cycle retardation of CNE-1 cells treated with 40 μmol/L nicotinamide for 48 h were detected by Annexin V-FITC/PI double staining flow cytometry. Cell migration and invasion were evaluated by transwell assay.Real-time fluorescent quantitative PCR and Western blot were used to detect the mRNA level and the expression of p53 and matrix metalloproteinases 9(MMP-9) proteins in CNE-1 cells. Results Compared with the blank control group, the data of CCK-8 assay showed that nicotinamide had an effective inhibition on the proliferation activity of CNE-1 cells(P<0.01), and the effect was in time-dose dependence manner. Flow cytometry results showed that the nicotinamide could promote apoptosis of CNE-1 cells treated with 40μmol/L nicotinamide for 48 h(P<0.01), with the number of cells increased in G2/M and decreased in G0/G1phase(P<0.05). And the migration and invasion were inhibited. Compared with the control group, the level of p53 protein was upregulated, while the level of MMP-9 protein decreasedwith 40 μmol/L nicotinamide treatment for 48 h. Conclusion Nicotinamide can inhibit the proliferation and promote the apoptosis of human nasopharyngeal carcinoma CNE-1 cells by up-regulating the expression of p53 protein and restoring the cell cycle, and also affect the expression of MMP-9 protein, thus reducing the migration and invasion ability of CNE-1 cells.