CAJ | 학술논문

目的：探讨整合素连接激酶（ILK）在非小细胞肺癌（NSCLC）中的表达及在侵袭和迁移中的作用和相关分子机制。方法：免疫组化法检测 ILK 蛋白在 NSCLC 患者中的表达，细胞转染、siRNA 干扰、细胞划痕试验、实时定量 PCR、Western blot 方法探讨 ILK 在肺癌 A549细胞中的表达及分子机制。结果：ILK 蛋白在原发性 NSCLC 组织中过度表达30.6%（33/108）并且和 TNM 分期（P ＝0.001）、淋巴结转移（ P ＝0.033）相关。ILK 在 A549细胞中过度表达并且通过下调 E - cadherin，上调波形蛋白、纤维连接蛋白、Snail、Slug 导致上皮-间质转化（EMT）。此外，NF -κB 抑制剂 BAY 11-7028和小干扰靶 RNA（siRNA）NF - P65可诱导 E - cadher-in 的表达下调。结论：ILK 在原发性 NSCLC 组织中高表达并与 TNM 分期和淋巴结转移相关，其促进肺癌细胞的侵袭和迁徙机制可能是经 NF -κB 信号通路诱导 EMT 所致。
목적：탐토정합소련접격매（ILK）재비소세포폐암（NSCLC）중적표체급재침습화천이중적작용화상관분자궤제。방법：면역조화법검측 ILK 단백재 NSCLC 환자중적표체，세포전염、siRNA 간우、세포화흔시험、실시정량 PCR、Western blot 방법탐토 ILK 재폐암 A549세포중적표체급분자궤제。결과：ILK 단백재원발성 NSCLC 조직중과도표체30.6%（33/108）병차화 TNM 분기（P ＝0.001）、림파결전이（ P ＝0.033）상관。ILK 재 A549세포중과도표체병차통과하조 E - cadherin，상조파형단백、섬유련접단백、Snail、Slug 도치상피-간질전화（EMT）。차외，NF -κB 억제제 BAY 11-7028화소간우파 RNA（siRNA）NF - P65가유도 E - cadher-in 적표체하조。결론：ILK 재원발성 NSCLC 조직중고표체병여 TNM 분기화림파결전이상관，기촉진폐암세포적침습화천사궤제가능시경 NF -κB 신호통로유도 EMT 소치。
Objective:To detect the exPression of integrin - linked kinase(ILK)in non - small cell lung cancer (NSCLC)and investigate the molecular mechanism in invasion and migration. Methods:The exPression of ILK was determined by means of immunohistochemistry in Patients with NSCLC. The exPression and molecular mechanism of ILK in A549 cells were studied by cell transfection,siRNA interference,cell scratch test,real - time quantitative PCR and Western blot. Results:The exPression rate of ILK was 30. 6%(33 / 108)in Primary NSCLC tissue that was asso-ciated with TNM staging(P = 0. 001)and lymPh node metastasis(P = 0. 033). ILK was over - exPressing in A549 cells and led to ePithelial mesenchymal transition(EMT)through down - regulating E - cadherin,uP - regulating vi-mentin,fibronectin,Snail and Slug. In addition,NF - κB inhibitor BAY 11 - 7028 and small interference target RNA (siRNA)NF - P65 could induce the down - regulation of E - cadherin. Conclusion:ILK was over - exPressed in NSCLC and associated with TNM staging and lymPh node metastasis. ILK Promotes lung cancer cell migration and in-vasion by inducing EMT through NF - κB signal Pathway.