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目的:探讨Survivin、Survivin-ΔEx3及VEGF在食管癌细胞诱导血管形成中作用的相关性。方法:用食管鳞癌肿瘤条件培养基培养人脐静脉内皮细胞,用ELISA法检测肿瘤条件培养基中VEGF蛋白的表达情况。用RT-PCR法检测内皮细胞中Survivin、Survivin-ΔEx3及VEGF的表达情况。结果:肿瘤条件培养基中VEGF蛋白表达随培养时间呈上升趋势。实验组人脐静脉内皮细胞中Survivin在更换肿瘤条件培养基后4及10h时表达明显增加,与对照组比较差异有统计学意义(CMvs RPMI:4h:1.019 7±0.058 8 vs 0.658 8±0.043 7,P=0.000 5;10 h:0.797 1±0.074 4 vs0.444 9±0.041 2,P=0.001 0),而Survivin-ΔEx3在实验组和对照组间的表达差异无统计学意义(CMvs RP-MI:4h:0.423 7±0.087 0 vs 0.294 0±0.043 1,P=0.109 1;10h:0.372 7±0.084 8 vs 0.226 4±0.009 2,P=0.078 1),VEGF在4及10h时表达明显下降,与对照组比较差异有统计学意义(CM vs RPMI:4h:0.276 7±0.065 8 vs 0.977 8±0.044 5,P=0.0000;10h:0.173 9±0.024 1 vs 0.917 8±0.124 7,P=0.004 8)。结论:食管癌肿瘤条件培养基可通过VEGF作用于人脐静脉内皮细胞表面的受体,进而增加人脐静脉内皮细胞中Survivin的表达,促进肿瘤新生血管形成,同时抑制血管内皮细胞中VEGF的表达,这为食管癌肿瘤血管形成的发生机制及防治提供一定的实验依据。
Objective: To investigate the correlation between Survivin, Survivin-ΔEx3 and VEGF in esophageal cancer-induced angiogenesis. Methods: Human umbilical vein endothelial cells were cultured in esophageal squamous cell carcinoma-conditioned medium and the expression of VEGF protein in tumor-conditioned media was detected by ELISA. The expression of Survivin, Survivin-ΔEx3 and VEGF in endothelial cells was detected by RT-PCR. Results: The expression of VEGF protein in tumor-conditioned media showed an upward trend with the incubation time. Survivin expression of human umbilical vein endothelial cells in the experimental group was significantly increased at 4 and 10 h after the tumor medium was changed, which was significantly different from the control group (CMvs RPMI: 4: 1.019 7 ± 0.058 8 vs 0.658 8 ± 0.043 7 , P = 0.0005; 10 h: 0.797 1 ± 0.074 4 vs0.444 9 ± 0.041 2, P = 0.001 0), while the expression of Survivin-ΔEx3 was not significantly different between the experimental group and the control group (CMvs RP- MI: 4h: 0.423 7 ± 0.087 0 vs 0.294 0 ± 0.043 1, P = 0.109 1; 10h: 0.372 7 ± 0.084 8 vs 0.226 4 ± 0.009 2, P = 0.078 1). The expression of VEGF was significantly decreased at 4 and 10 h , And the difference was statistically significant compared with the control group (CM vs RPMI: 4h: 0.276 7 ± 0.065 8 vs 0.977 8 ± 0.044 5, P = 0.0000; 10h: 0.173 9 ± 0.024 1 vs 0.917 8 ± 0.124 7, P = 0.004 8). CONCLUSION: The conditioned medium of esophageal cancer can act on the surface receptors of human umbilical vein endothelial cells by VEGF, and then increase the expression of Survivin in human umbilical vein endothelial cells, promote tumor angiogenesis and inhibit the expression of VEGF in vascular endothelial cells , Which provide some experimental evidences for the pathogenesis and prevention of esophageal carcinoma tumor angiogenesis.