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目的 了解甲状腺滤泡状癌细胞中导入内皮抑素 (Endostatin ,ES)基因对体内外生长的影响 ,并探讨其作用机制。方法 用逆转录病毒载体将ES基因导入FTC133 细胞中 ,采用RT PCR和ELISA检测导入基因在肿瘤细胞的表达。观察肿瘤在裸鼠模型中的生长状况。用抗CD31抗体对肿瘤切片进行免疫组织化学染色检测微血管 ,计算微血管密度 (microvesseldensity ,MVD)。检测血清中ES和VEGF浓度。 结果 顺利将ES基因导入到FTC13 3 中得到稳定表达ES的肿瘤细胞系FTC133 rvEndo。后者在体外增值速度与母系相似。而在裸鼠模型中 ,其肿瘤生长速度明显慢于母系。种植 33天后 ,FTC133 组肿瘤大小为 ( 30 0 2± 44 1)mm3,FTC13 3 rvEndo组为 ( 5 5 7± 15 2 )mm3,两组间差异有显著性 (P =0 0 0 0 2 )。免疫组化染色表明FTC133 rvEndo肿瘤中血管内皮细胞数明显减少 ,MVD为 34 86± 10 6 8;而对照组为 6 4 71± 17 0 5 ,差异有显著性 (P =0 0 0 2 0 )。带瘤鼠血清人VEGF浓度FTC133 rvEndo组为 ( 8 99± 0 6 5 )ng/L ,明显低于对照组 ( 2 9 34± 5 5 5 )ng/L( P =0 0 0 98)。结论 利用逆转录病毒载体可将ES基因转入甲状腺滤泡状癌细胞系中 ,该基因的导入通过抑制血管生成使肿瘤体内生长速度减慢。其机制可能与抑制肿瘤细胞?
Objective To investigate the effect of endostatin (ES) gene on the growth of thyroid follicular carcinoma cells in vitro and in vivo, and to explore its mechanism. Methods The ES gene was introduced into FTC133 cells by retroviral vector and the expression of the introduced gene in tumor cells was detected by RT PCR and ELISA. The growth of the tumor in the nude mouse model was observed. Tumor sections were examined by immunohistochemistry with anti-CD31 antibody for the detection of microvessels, and the microvessel density (MVD) was calculated. Serum ES and VEGF concentrations were measured. As a result, the ES gene was successfully introduced into FTC133 to obtain a stable ES cell line FTC133 rvEndo. The latter rate of increase in vitro and maternal similar. In the nude mouse model, the tumor growth rate was significantly slower than the maternal. After 33 days of implantation, the tumor size in FTC133 group was (30 0 2 ± 44 1) mm 3 and in FTC13 3 rvEndo group was (57 57 ± 15 2) mm 3, with significant difference between the two groups (P = 0.00002) . Immunohistochemical staining showed that the number of vascular endothelial cells in the FTC133 rvEndo tumor was significantly reduced, with a MVD of 34 86 ± 10 6 8, while the control group was 6 4 71 ± 17 0 5 (P = 0.0020) . The serum concentration of VEGF in the tumor-bearing mice was (899 ± 0.05) ng / L in the FTC133 rvEndo group, which was significantly lower than that in the control group (2934 ± 555) ng / L (P = 0.0098). CONCLUSIONS: The ES gene can be transferred into thyroid follicular carcinoma cell line by retroviral vector. The introduction of this gene can slow the growth of tumor in vivo by inhibiting angiogenesis. The mechanism may be related to the inhibition of tumor cells?