DLC-1过表达对非小细胞肺癌细胞增殖和侵袭的影响

目的 探讨肝癌缺失基因1（deleted in liver cancer-1, DLC-1）对非小细胞肺癌（non-small cell lung cancer，NSCLC）细胞增殖和侵袭的影响及其作用机制。方法 构建pcDNA3.1-DLC-1重组质粒并转染至人非小细胞肺癌A549和Calu-6细胞，采用Western blot检测DLC-1蛋白表达，qRT-PCR检测DLC-1和ROCK1 mRNA表达，平板克隆形成实验检测细胞增殖能力，流式细胞仪检测细胞周期，Transwell实验检测细胞侵袭能力。结果 A549和Calu-6细胞转染pcDNA3.1-DLC-1重组质粒后，DLC-1蛋白和mRNA表达量均高于对照组（均P<0.05）。与对照组相比，DLC-1过表达后A549和Calu-6细胞中的ROCK1 mRNA表达量降低（均P<0.05），细胞增殖能力下降（均P<0.05）；A549细胞周期被阻滞于G1期，侵袭能力下降（P<0.05）。结论 DLC-1过表达可抑制NSCLC细胞增殖和侵袭，其作用机制可能与靶向调控ROCK1有关。

Effect of DLC-1 overexpression on proliferation and invasion of non-small cell lung cancer

Objective  To investigate the effect of deleted in liver cancer-1 (DLC-1) on proliferation and invasion of non-small cell lung cancer (NSCLC) cells and its mechanism. Methods The recombinant plasmid pcDNA3.1-DLC-1 was constructed and transfected into  human non-small cell lung cancer cell lines A549 and Calu-6. The protein expression of DLC-1 was detected by Western blot. The mRNA expression of DLC-1 and ROCK1 was detected by qRT-PCR. The cell proliferation ability was detected by the plate clone formation test. The cell cycle was detected by the flow cytometry. The invasion ability of cells was detected by Transwell. Results After the A549 and Calu-6 cells were transfected with recombinant plasmid pcDNA3.1-DLC-1, the protein and mRNA expression levels of DLC-1 were higher than those of the control group (all P<0.05). Compared with the control group, the mRNA expression of ROCK1 in A549 and Calu-6 cells was reduced after the over-expression of DLC-1 (all P<0.05), and the cell proliferation ability was decreased (all P<0.05). The A549 cell cycle was arrested in the G1 phase, and the invasion ability was decreased (P<0.05). Conclusions The over-expression of DLC-1 can inhibit the proliferation and invasion of NSCLC cells, and its mechanism may be related to the targeted regulation of ROCK1.