CAJ | 학술논문

目的：探讨在顺铂作用下的A549细胞中JNK信号通路与肺耐药蛋白LRP之间的相互关系。方法：用SP600125抑制JNK信号通路的活化，CCK-8法检测顺铂药物敏感性，流式细胞术检测细胞凋亡率，用Western blotting法检测LRP、JNK、P-JNK的表达。结果：顺铂可活化JNK信号通路，上调LRP的表达；用SP600125抑制JNK信号通路后，LRP的表达下调，增强了顺铂化疗敏感性，促进了细胞凋亡。结论：在A549细胞中，活化的JNK信号通路上调LRP的表达促进化疗耐药，因此阻断JNK信号通路为肺癌提供新的治疗靶点。
목적：탐토재순박작용하적A549세포중JNK신호통로여폐내약단백LRP지간적상호관계。방법：용SP600125억제JNK신호통로적활화，CCK-8법검측순박약물민감성，류식세포술검측세포조망솔，용Western blotting법검측LRP、JNK、P-JNK적표체。결과：순박가활화JNK신호통로，상조LRP적표체；용SP600125억제JNK신호통로후，LRP적표체하조，증강료순박화료민감성，촉진료세포조망。결론：재A549세포중，활화적JNK신호통로상조LRP적표체촉진화료내약，인차조단JNK신호통로위폐암제공신적치료파점。
Objective: To investigate the relationship between the c-Jun N-terminal kinase (JNK) pathway and lung-resistance protein (LRP). Methods:A549 cells were treated with various concentrations of CDDP for 72 h. The LRP mRNA expression was then analyzed using reverse transcription PCR (RT-PCR). LRP, JNK, and P-JNK were analyzed by Western blotting. The A549 cells were then pretreated with SP600125 (2 μg/ml to 4 μg/ml ) for 1 h. Afterward, CDDP (16 μg/ml) was added into the culture for 72 h. A Cell Counting Kit-8 was used to investigate the sensitivity of CDDP to the A549 cells. Flow cytometry was used to detect the apoptosis rate. The LRP mRNA expression was analyzed using RT-PCR. LRP, JNK, and P-JNK were analyzed by Western blotting. Results:CDDP in-duced the mRNA and protein expression of both LRP and P-JNK in a dose-dependent manner. Pretreatment with SP600125 enhanced the sensitivity of CDDP to the A549 cells and increased the apoptosis rate. However, the LRP mRNA and LRP expression in the pre-treated cells was lower than that in the presence of CDDP alone. Conclusion:In A549 cells, CDDP induces the LRP expression via the JNK pathway. This result suggests that lung cancer therapy can be improved by the addition of CDDP to inhibit the JNK signaling path-way.