CAJ | 학술논문

目的探讨肺耐药相关蛋白(LRP)、血管内皮生长因子(VEGF)及微血管密度(MVD)在非小细胞肺癌(NSCLC)中的变化、相互关系及可能的机制.方法应用免疫组化技术检测56例NSCLC癌组织和27例正常对照肺组织中LRP、VEGF表达及MVD情况.结果 ①LRP阳性表达分布于癌细胞胞浆内,表达率66.1%,显著高于对照肺组织(P<0.01),其显著性与病理类型无关;NSCLC组LRP的表达在不同性别、TNM分期、有无淋巴结转移及两年生存率的比较上均无明显统计学意义(P>0.05).②与对照组比较,NSCLC组VEGF表达明显升高(P<0.01),其显著性与病理类型无关.NSCLC组VEGF表达与TNM分期、有无淋巴结转移相关(P<0.05).③NSCLC组MVD明显高于对照组(P<0.01),其显著性不受病理类型、病理分级的影响.MVD在Ⅲ+Ⅳ期肺癌中为18.5±5.8,明显高于Ⅰ期的13.8±5.1(P<0.05),有淋巴结转移的高于无淋巴结转移者(P<0.05),两年存活的MVD低于两年死亡的MVD(P<0.01).④NSCLC组VEGF、LRP高表达和MVD增高具有一致性(P<0.05).结论非小细胞肺癌血管生成与肺耐药相关基因具有一定的相关性.LRP的高表达可能与VEGF上调其基因及VEGF促进肿瘤MVD增加有关.抑制肿瘤新生血管的生成有望降低甚或遏制对非小细胞肺癌化疗的耐药性.
목적 탐토폐내약상관단백(LRP)、혈관내피생장인자(VEGF)급미혈관밀도(MVD)재비소세포폐암(NSCLC)중적변화、상호관계급가능적궤제.방법 응용면역조화기술검측56례NSCLC암조직화27례정상대조폐조직중LRP、VEGF표체급MVD정황.결과 ①LRP양성표체분포우암세포포장내,표체솔66.1%,현저고우대조폐조직(P<0.01),기현저성여병리류형무관;NSCLC조LRP적표체재불동성별、TNM분기、유무림파결전이급량년생존솔적비교상균무명현통계학의의(P>0.05).②여대조조비교,NSCLC조VEGF표체명현승고(P<0.01),기현저성여병리류형무관.NSCLC조VEGF표체여TNM분기、유무림파결전이상관(P<0.05).③NSCLC조MVD명현고우대조조(P<0.01),기현저성불수병리류형、병리분급적영향.MVD재Ⅲ+Ⅳ기폐암중위18.5±5.8,명현고우Ⅰ기적13.8±5.1(P<0.05),유림파결전이적고우무림파결전이자(P<0.05),량년존활적MVD저우량년사망적MVD(P<0.01).④NSCLC조VEGF、LRP고표체화MVD증고구유일치성(P<0.05).결론 비소세포폐암혈관생성여폐내약상관기인구유일정적상관성.LRP적고표체가능여VEGF상조기기인급VEGF촉진종류MVD증가유관.억제종류신생혈관적생성유망강저심혹알제대비소세포폐암화료적내약성.
Objective To investigate the changes in lung resistance-related protein (LRP) and vascular endothelial growth factor (VEGF) expressions and micro-vessel density (MVD) in non-small cell lung cancer (NSCLC), and to elucidate their possible relationship and mechanism. Methods Immunohistochemistry was used to detect changes in LRP and VEGF expressions, and MVD level in lung tissues of 56 NSCLC cases and 27 normal controls. Results ① LRP expression (66.1%) was concentrated in the cytoplasm of cancer cells, which was significantly higher than that in lung tissues of control group (P<0.01); the significance was not related to the pathological type. There was no significant difference in LRP expression among gender, TNM stage, lymph node metastasis, and two-year survival in NSCLC (P>0.05). ② In comparison to the control group, NSCLC group had significantly increased VEGF expression (P<0.01), which was not related to the pathological type. VEGF expression in NSCLC group had a significant association with TNM stage and lymph node metastasis (P<0.05). ③ The NSCLC group had a significantly higher MVD than the control group (P<0.01), which was not affected by the pathological type or degree. MVD value (18.5±5.8) of stage Ⅲ and Ⅳ in NSCLC group was significantly higher than that (13.8±5.1) of stage Ⅰ (P<0.05); MVD value for patients with lymph node metastasis was higher than that without lymph node metastasis (P<0.05); MVD value for patients with two-year survival was less than those who died within two years (P<0.01). ④ NSCLC group with high VEGF and LRP expressions had a consistently increased MVD value (P<0.05). Conclusion There is a certain relationship between tumor angiogenesis and LRP expression in NSCLC. VEGF is responsible for the high expression of LRP through up-regulating LRP gene and augmenting tumor MVD. Inhibition of angiogenesis in tumor is expected to reduce or inhibit drug resistance to NSCLC.