TFPI-2、VEGF在非小细胞肺癌中的表达及相关性研究

目的研究组织因子途径抑制物-2(tissue factor pathway inhibitor-2,TFPI-2)、血管内皮生长因子(vascular endotheli-al growth factor,VEGF)在非小细胞肺癌(non-small cell lung cancer,NSCLC)中的表达及其间的相关性。方法采用免疫组化法检测60例NSCLC组织TFPI-2、VEGF的表达及CD31单克隆抗体标记的微血管密度(MVD)。结果 NSCLC中临床分期为Ⅰ、Ⅱ、Ⅲ期的患者中TFPI-2表达阳性率分别为75.8%、25.0%和40.0%(P=0.003),无淋巴结转移和有淋巴结转移的患者中TF-PI-2表达阳性率分别为66.7%、38.1%(P=0.033)。临床分期为Ⅰ、Ⅱ、Ⅲ期的患者中EVGF表达阳性率分别为60.6%、88.3%和93.3%(P=0.040),无淋巴结转移和有淋巴结转移的患者中VEGF表达阳性率分别为64.1%、90.5%(P=0.028)。NSCLC组织中的TFPI-2的表达与VEGF的表达呈负相关(r=-0.351),差异有统计学意义(P=0.004)。高、低MVD组中的TFPI-2阳性表达率分别为41.2%、76.9%(P=0.006)。高、低MVD组中的VEGF阳性表达率分别为76.5%、30.87%(P=0.000)。结论 NSCLC中TFPI-2可能通过下调VEGF的表达抑制肿瘤新生血管的形成,从而抑制NSCLC的生长、浸润及转移。

Expression and correlation of TFPI-2 and VEGF in non-small cell lung cancer

Objective To investigate the relationship between the expression and correlation of TFPI-2 and VEGF in patients with non-small cell lung cancer （NSCLC）. Methods The expression of TFPI-2, VEGF and MVD, marked with CD31, were detected by im- munohistochemistry in 60 patients with NSCLC. Results The expression positive rate of TEPI-2 in patients with NSCLC at clinical stage Ⅰ、Ⅱ、Ⅲ was 75.8%, 25.0% and 40.0% respectively （ P = 0. 003 ） , and the expression positive rate of TEPI-2 in patients with and without lymph node metastasis was 66. 7% and 38.1% respectively （ P = 0. 033 ）. The expression positive rate of EVGF in patients with NSCLC at clinical stage Ⅰ、Ⅱ、Ⅲ was 60. 6%, 88.3% and 93.3% respectively （ P = 0. 040）, and the expression positive rate of VEGF in patients with and without lymph node metastasis was 64. 1% and 90. 5% respectively （P =0. 028）. The expression of TFPI-2 and VEGF in NSCLC patients were negatively correlated with statistical significance （ r =0. 3,51, P =0. 004）. The expression positive rate of TFPI-2 was 41.2% and 76. 9% respectively in the high MVD group and the low MVD group （P =0. 006）, and he expression positive rate of TFPI-2 was 76. 5 % and 30. 87% respectively in the high MVD group and the low MVD group （ P = 0. 000）. Conclusion TFPI- 2 may inhibit the angiogenesis of NSCLC by reducing the expression of VEGF.