HIF-1α、VEGF、VEGFR2在非小细胞肺癌组织中的表达及临床意义

Expressions of HIF-1α、VEGF and VEGFR2 in Non-small Cell Lung Cancer and their Clincical Significance

目的探讨非小细胞肺癌(NSCLC)病理组织中乏氧诱导因子-1α(HIF-1α)、血管内皮生长因子(VEGF)、血管内皮生长因子受体2(VEGFR2)的表达情况及临床意义。方法采用免疫组化方法测定50例非小细胞肺癌组织和10例肺良性病组织中HIF-1α、VEGF、VEGFR2表达情况,并结合患者的临床病理资料进行分析。结果 50例非小细胞肺癌组织中HIF-1α、VEGF、VEGFR2高表达率分别为58%、54%、60%。三者在非小细胞肺癌组织中均有高表达,与对照组比较差异有显著性(P<0.01)。HIF-1α、VEGF、VEGFR2表达与肿瘤的TNM分期、淋巴结转移和肿瘤组织分化程度有关(P<0.05),而与患者年龄、性别、病理类型无关(P>0.05)。HIF-1α的表达与VEGF、VEGFR2表达呈显著正相关(P<0.01)。结论非小细胞肺癌中HIF-1α、VEGF、VEGFR2表达水平有相关性,它们在非小细胞肺癌发生、发展和转移中有重要意义,对临床判断非小细胞肺癌预后和指导临床抗血管生成有一定的价值。

Objective To investigate the correlation between the expressions of hypoxia inducible factor 1α（HIF-1α）,vascular endothelial growth factor（VEGF）and vascular endothelial growth factor receptor 2（VEGFR2）in human non-small cell lung cancer and their clinical significance.Methods The expression of HIF-1α、VEGF and VEGFR2 were detected by immunohistochemistry in 50 patients with non-small cell lung cancer and 10 patients with benign lesion of lung.some clinicopathologic parameters was analyzed.Results Positive immunostaining rates of HIF-1α、VEGF and VEGFR2 were 58%、54% and 60% respectively.Being compared with the conrtol,the expression of HIF-1α、VEGF and VEGFR2 in lung cancer was significantly different（P0.01）.The relation between those protein expression and the clinicopathologic character of NSCLC：no difference were discovered in the expression of these protein when the age 、gender and pathology type were considered（P0.05）.But on the other hand,there were difference when the histological grade,clinical TNM stage and the lymph node status were considered（P0.05）.In the result analysis by Spearman Test,the expression of HIF-1α shows significantly positive correlation with that of VEGF and VEGFR2（P0.01）.Conclusion According to these data,we can speculate that HIF-1α、VEGF and VEGFR2 correlate significantly and play a key role in NSCLC occuring,development,metastatsis and prognosis,it will be benefit to clinical treatment of antiangiogenesis.