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为探讨S100A8和S100A9对鼻咽癌细胞系CNE2的影响及是否通过Wnt/β-catenin通路而发挥作用,以培养基添加1μg/m L S100A8/S100A9培养CNE2为实验组,采用划痕、黏附和平板克隆实验分别检测S100A8/S100A9对CNE2细胞的生物学行为影响,同时运用Western blotting检测CNE2细胞中β-catenin蛋白的累积。实验结果显示,S100A8/S100A9起促进CNE2细胞迁移(p<0.05,p<0.01)、基质黏附(p<0.01)和平板克隆(p<0.01)的作用,且添加S100A8/S100A9蛋白后1 h,CNE2细胞中β-catenin的累积明显上调。以上结果显示S100A8/S100A9可促进鼻咽癌细胞CNE2侵袭和迁移及细胞干性增强等生物学行为,其机制可能有Wnt/β-catenin通路的参与。
In order to investigate the effect of S100A8 and S100A9 on nasopharyngeal carcinoma cell line CNE2 and whether through Wnt / β-catenin pathway, CNE2 was cultured in the medium supplemented with 1μg / ml S100A8 / S100A9 as experimental group, The effects of S100A8 / S100A9 on the biological behavior of CNE2 cells were detected by plate clone assay, and the accumulation of β-catenin protein in CNE2 cells was detected by Western blotting. The results showed that S100A8 / S100A9 could promote the migration of CNE2 cells (p <0.05, p <0.01), matrix adhesion (p <0.01) and plate clone (p <0.01) The accumulation of β-catenin in CNE2 cells was significantly up-regulated. The above results show that S100A8 / S100A9 can promote the invasion and migration of CNE2 cells and enhance the cell viability and so on. Its mechanism may involve the Wnt / β-catenin pathway.