CAJ | 학술논문

目的检测窖蛋白1(Car-1)在非小细胞肺癌(NSCLC)中的蛋白表达以及启动子的甲基化状况,探讨Cav-1基因在NSCLC中的作用及其临床意义.方法应用免疫组织化学(sP法)和量子点Qd600染色检测123例NSCLC组织、17例良性病变肺组织中Cav一1蛋白表达和亚细胞定位.亚硫酸氢钠处理DNA,甲基化特异性PCR(MSP)检测Cav-1基因启动子区域的甲基化水平.结果 Cav-1蛋白在肺支气管黏膜上皮细胞、肺泡上皮细胞、毛细血管内皮细胞、成纤维细胞、平滑肌细胞的胞质和胞膜高表达.癌旁组织(对照)组和肺癌组中Cav-1蛋白的阳性率分别为17/17、43.1%(53/123),两组间差异有统计学意义(P=0.001);Cav-1蛋白在NSCLC不同的组织学类型(P=0.552)和分化程度(P=0.160)中差异均无统计学意义.Cav-1蛋白阳性率与NSCLC的TNM分期(P=0.001)以及淋巴结转移(P=0.001)均相关.在40例Cav-1蛋白表达为阴性的肺癌组织和12例癌旁肺组织,MSP法均未检测到Cav-1因启动子区域的甲基化.结论 Cav-1蛋白失表达的机制可能与启动子区是否甲基化无关.Cav-1蛋白高表达预示NSCLC恶化进展和高侵袭性.
목적 검측교단백1(Car-1)재비소세포폐암(NSCLC)중적단백표체이급계동자적갑기화상황,탐토Cav-1기인재NSCLC중적작용급기림상의의.방법 응용면역조직화학(sP법)화양자점Qd600염색검측123례NSCLC조직、17례량성병변폐조직중Cav일1단백표체화아세포정위.아류산경납처리DNA,갑기화특이성PCR(MSP)검측Cav-1기인계동자구역적갑기화수평.결과 Cav-1단백재폐지기관점막상피세포、폐포상피세포、모세혈관내피세포、성섬유세포、평활기세포적포질화포막고표체.암방조직(대조)조화폐암조중Cav-1단백적양성솔분별위17/17、43.1%(53/123),량조간차이유통계학의의(P=0.001);Cav-1단백재NSCLC불동적조직학류형(P=0.552)화분화정도(P=0.160)중차이균무통계학의의.Cav-1단백양성솔여NSCLC적TNM분기(P=0.001)이급림파결전이(P=0.001)균상관.재40례Cav-1단백표체위음성적폐암조직화12례암방폐조직,MSP법균미검측도Cav-1인계동자구역적갑기화.결론 Cav-1단백실표체적궤제가능여계동자구시부갑기화무관.Cav-1단백고표체예시NSCLC악화진전화고침습성.
Objective To study the methylation of CpG islands in the promoter region, expression of caveolin 1(Cav-1)gene and their clinical significance in non. small cell lung cancers(NSCLC). Methods Immunohistochemistry and quanta Qd600 staining were used to detect the expression of Cav-1 in tissues from benign lung lesions(n=17)and NSCLC(n=123). DNA was treated with sodium bisulfite and the Cav-1 promoter region was screened using methylation. specmc polymerase chain reaction for the possible methylation sites. Results Cav. 1 protein was highly expressed in cytoplasm and cell membrane of normal bronchial epithelium, alveolar epithelium, endothelial cells. fibroblasts and smooth muscle cells. The expression rates of Cav-1 protein were 100%(17/17)in the control group and 43. 1%(53/123)in the NSCLC group(P=0. 001). Amongst the NSCLC group, there was no statistically significant difference in Cav-1 protein expression in different histologic types(P=0. 552)and tumor grades(P=0. 160). 0n the other hand, Car-1 protein immunoreactivity was remarkably higher in advanced tumor stage:72. 7%in stage ⅢA+ⅢB, compared with 9. 4% in stage IA+IB and 38. 3%in stageⅡA+ⅡB(P=0. 001). The expression rate of Cav-1 protein in the NSCLC cases with lymph node metastasis was 53. 6%. compared with 20. 5%in those without nodal involvement(P=0. 001). DNA from 40 NSCLC cases with negative Cav-1 protein expression and 12 cases of pefitumoral lung tissues were extracted. Methylation in the promoter region of Car-1 gene was not detected in lung cancer or peritumoral tissues. Conclusions High expression of Cav1 protein is respected of the aggressive clinical behavior and advanced tumor stage. Loss of Cav-1 protein expression seems not correlated to the methylation status in the promoter region of Cav-1 gene.