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目的探讨过氧化物酶体增殖因子激活受体α激动剂非诺贝特对人肺癌A549细胞生长、迁移侵袭能力的影响及其可能机制。方法体外培养人肺癌A549细胞,分别用0、12.5、25、50、75、100μmol/L非诺贝特处理细胞,阴性对照组为0μmol/L非诺贝特浓度组;MTT法检测不同药物浓度作用下肺癌A549细胞的生长抑制情况;细胞划痕实验和Transwell侵袭实验检测非诺贝特对肺癌A549细胞迁移及侵袭运动能力的影响,RT-PCR法检测A549细胞中PPARα(Peroxisome Proliferator-Activated Receptors alpha)、MMP-2(Matrix Metalloproteinase-2)、MMP-9、Timp-1(tissue inhibitor of metalloproteinase-1)、Timp-2m RNA的表达情况。结果非诺贝特能够抑制A549细胞生长,呈时间-剂量关系(P<0.05);细胞划痕实验及Transwell侵袭实验结果显示非诺贝特能够降低A549细胞的迁移侵袭能力;RT-PCR结果提示非诺贝特能够上调PPARα、Timp-1、Timp-2m RAN表达,下调MMP-2、MMP-9 m RNA表达,差异有统计学意义(P<0.05)。结论非诺贝特能够抑制肺癌A549细胞生长、迁移及侵袭能力,其机制可能与PPARα、MMPs、Timps有关。
Objective To investigate the effect and mechanism of peroxisome proliferator-activated receptor α agonist fenofibrate on the growth, migration and invasion of human lung cancer A549 cells. Methods Human lung adenocarcinoma A549 cells were cultured in vitro. The cells were treated with fenofibrate at 0, 12.5, 25, 50, 75 and 100 μmol / L, respectively. The negative control group was 0 μmol / L fenofibrate. MTT assay was used to detect the concentration of different drugs A549 cells were treated with fenofibrate and transwell invasion assay. The effect of fenofibrate on the migration and invasion of lung cancer A549 cells was detected by flow cytometry. The expression of PPARα (Peroxisome Proliferator-Activated Receptors alpha, MMP-2, MMP-9, Timp-1 and Timp-2m RNA expression. Results Fenofibrate could inhibit the growth of A549 cells in a dose-time-dependent manner (P <0.05). The results of cell scratch assay and Transwell invasion assay showed that fenofibrate could reduce the migration and invasion ability of A549 cells. The results of RT- Fenofibrate could up-regulate the expression of PPARα, Timp-1 and Timp-2m RAN, and down-regulate the expression of MMP-2 and MMP-9 mRNA. The difference was statistically significant (P <0.05). Conclusion Fenofibrate can inhibit the growth, migration and invasion of lung cancer A549 cells. The mechanism may be related to PPARα, MMPs and Timps.