非小细胞肺癌组织ET-1、VEGF及MVD的表达及相互关系

Expression of endothelin,vascular endothelial growth factor and microvessel density in non-small cell lung cancer tissue

目的:研究非小细胞肺癌(NSCLC)组织中内皮素-1(ET-1)、血管内皮生长因子(VEGF)的表达和微血管密度(MVD),以探讨ET-1、VEGF在肺癌组织血管形成中的调节作用。方法:采用免疫组化和图像分析技术,检测40例NSCLC组织标本中ET-1、VEGF的表达及MVD。结果:ET-1、VEGF在NSCLC组织表达率分别为55%(22/40)、62%(25/40),显著高于肺良性病变组8%(1/12)、0%(0/12)及正常对照组(0/10)、(0/10)(P<0.01);ET-1、VEGF表达阳性组MVD(26.23±3.52、23.40±5.29)显著高于ET-1、VEGF表达阴性组(15.46±4.85、16.40±3.85);ET-1、VEGF表达和MVD在低、中、高分化癌中存在显著差异[ET-1(0.212±0.031vs0.147±0.015vs0.103±0.032)、VEGF(0.267±0.023vs0.166±0.021vs0.112±0.012)、MVD(26.75±3.20vs23.14±3.38vs16.15±3.22)](P<0.01或P<0.05);淋巴结转移阳性组ET-1、VEGF表达和MVD值显著高于阴性组[ET-1(0.198±0.037vs0.141±0.032)、VEGF(0.256±0.022vs0.154±0.037)、MVD(27.62±3.58vs17.13±3.13)](P<0.01或P<0.05)。结论:ET-1、VEGF调控肺癌组织血管形成,促进肿瘤的生长和转移。

Objective：To explore the formation of blood vessels in non -small cell lung cancer（NSCLC） and the expression of endothelin - 1 （ ET - 1 ）, vascular endothelial growth factor （VEGF） and microvessel density （ MVD ） in NSCLC. Methods ： ET - 1, VEGF expression and MVD were detected by immuno - histochemistry and image analysis technique in 40 cases of NSCLC tissue. Results： The ET - 1, VEGF positive expression were mainly located in the cytoplasm of lung cancer. The positive rate of ET - 1, VEGF in NSCLC was significantly higher than that in normal and benign lesion （55% vs 8% vs 0% and 62% vs 0% vs 0% ） （P 〈0.01）. MVD was notably higher in ET - 1 ,VEGF positive expression tissues （26.23 ± 3.52 vs 15.46 ± 4.85,23.40 ± 5.29 vs 16.40 ± 3.85 ） （ P 〈 0.01 ）. ET - 1, VEGF and MVD expression in low and middle and high differentiation lung cancer were significantly different [ ET - 1（0.212±0.031 vs0.147 ±0.015 vs0. 103 ±0.032）, VEGF （ 0. 267 ± 0. 023 vs0.166±0.021 vs0.112 ± 0.012）and MVD（26.75 ± 3.20 vs 23. 14 ± 3.38 vs 16.15 ± 3.22） ] （P 〈 0.01 or P 〈 0.05 ）. ET - 1, VEGF expression and the MVD value of lymph node postitive group were remarkably higher than that of the negative group. Conclusion： ET - 1, VEGF may contribute to neovascularization of lung cancer as a angiogenic regulator and might play an important role in tumor angiogenesis.