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目的观察体外缺氧条件下骨肉瘤SaOS-2生物学特性的改变。方法建立骨肉瘤细胞体外缺氧培养模型;流式细胞仪分析细胞周期改变;划痕损伤法和Boyden侵袭小室检测细胞体外侵袭迁移能力的变化;半定量逆转录-聚合酶链反应(RT-PCR)和免疫组织化学(SP法)观察缺氧培养不同时相(8、16、24 h)血管内皮生长因子(VEGF)的表达。结果缺氧培养16 h内,细胞周期表现为G_1期阻滞。24 h后,细胞周期恢复常氧状态。缺氧培养24 h后,骨肉瘤细胞体外迁移和侵袭能力明显增强。缺氧处理后,VEGF mRNA以及蛋白的表达在缺氧条件下均显著增强。结论骨肉瘤细胞存在缺氧耐受机制,通过一系列生物学特性的改变来应对缺氧带来的不利。
Objective To observe the changes of biological characteristics of SaOS-2 osteosarcoma in vitro under hypoxia conditions. Methods The cell model of osteosarcoma cells was established by hypoxia in vitro. The changes of cell cycle were analyzed by flow cytometry. The invasion and migration of cells were detected by scratch injury method and Boyden invasion chamber. The semi-quantitative reverse transcriptase-polymerase chain reaction ) And immunohistochemistry (SP method) were used to observe the expression of vascular endothelial growth factor (VEGF) in different phases of hypoxia culture (8,16,24 h). Results Within 16 h hypoxia, the cell cycle showed G_1 phase arrest. After 24 h, the cell cycle returned to normoxia. After 24 h hypoxia, the ability of osteosarcoma cells to migrate and invade in vitro was significantly enhanced. After hypoxia treatment, the expression of VEGF mRNA and protein were significantly increased in hypoxia. Conclusion Osteosarcoma cells have hypoxia tolerance mechanism and respond to the adverse effects of hypoxia through a series of biological changes.