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目的:观察p53基因在骨肉瘤血管生成中的作用并探讨其作用。方法:采用3×10n 4接种数量的人共基底膜毛细血管形成试验模拟体内血管生成，应用免疫印迹及免疫荧光观察肌动蛋白纤维内蛋白水平及分布。最终使用免疫组织化学方法对196例人骨肉瘤临床样本检测S2448p哺乳动物类雷帕霉素靶蛋白(mTOR)的表达。采用独立样本n t检验。n 结果:观察到p53基因对骨肉瘤MG63细胞系的抑制作用明显，当p53浓度接近100 nmol/L时，其可以抑制人工基底膜上hFOB1.19细胞系内50%的血管生成；而当浓度大于200 nmol/L时，p53几乎可以完全抑制血管的生成血管分支点(2.37±1.56)个，低于0 nmol/L组的(26.79±3.24)个，差异有统计学意义(n t＝2.796，n P<0.05)。在41.8%(82/196)的样本中观察到血管内皮细胞中S2448P-mTOR的表达，经验证抑制作用源于p53基因对包括蛋白激酶B(Akt)、mTOR在内的磷脂酰肌醇3激酶(PI3K)下游因子磷酸化的抑制作用。n 结论:p53基因能够通过PI3K/Akt/mTOR信号通路抑制骨肉瘤的血管形成。“,”Objective:To investigate the role of p53 in the angiogenesis of osteosarcoma.Methods:The human co-basement membrane capillary formation test was used to simulate angiogenesis n in vivo with a 3×10n 4 density. The protein level and distribution of actin fibers were observed by Western blotting and immunofluorescence. Immunohistochemistry was used to detect the expression of S2448p mammalian target of rapamycin (mTOR) in 196 clinical samples of human osteosarcoma.n Results:The p53 gene had a significant inhibitory effect on the osteosarcoma MG63 cell line. When the p53 concentration was close to 100 nmol/L, it could inhibit 50% of the angiogenesis in the hFOB1.19 cell line on the artificial basement membrane, and when the concentration was greater than 200 nmol/L, p53 could almost completely inhibit angiogenesis. There were (2.37±1.56) branch points of blood vessels, which were significantly less than (26.79±3.24) in the 0 nmol/L group (n t=2.796, n P<0.05). The expression of S2448P-mTOR in vascular endothelial cells was detected in 41.8% (82/196) of the samples. It has been verified that the inhibitory effect was derived from the inhibitory effect of p53 gene on the phosphorylation of phosphoinositide 3-kinase (PI3K) downstream factors including protein kinase B (Akt) and mTOR.n Conclusion:These results show that p53 suppresses angiogenesis of osteosarcoma through inhibiting the PI3K/Akt/mTOR pathway.