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目的:研究转录因子WSTF对肺癌细胞增殖和侵袭作用的影响。方法:采用慢病毒介导的基因转染方法建立A549细胞WSTF高表达细胞系A549-WSTF和空质粒对照细胞系A549-control。细胞增殖实验和克隆形成实验观察ING5过表达对肺癌A549细胞增殖能力的影响;Trans-well迁移实验和侵袭实验观察WSTF对肺癌细胞迁移和侵袭能力的影响。结果:Western blot验证A549-WSTF细胞WSTF蛋白水平显著高于对照细胞A549-control,P=0.0004。WSTF高表达明显促进了肺癌细胞的增殖能力(1-4天P值分别为0.002、0.0004、0.0002和3.21×10-5)和克隆形成能力(P=0.004);WSTF过表达还显著促进了肺癌细胞从trans-well小室迁移到下室的作用,其OD570值分别为0.626±0.013(A549-WSTF)和0.322±0.010(A549-control),P=2.37×10-5;WSTF还促进肺癌细胞穿透基质胶迁移到下室,其OD570值分别为0.600±0.027(A549-WSTF)和0.333±0.017(A549-control),P=0.0004。结论:WSTF可以促进肺癌细胞的增殖和侵袭能力而发挥促癌作用。
Objective: To study the effect of transcription factor WSTF on the proliferation and invasion of lung cancer cells. Methods: A549-WSTF and A549-control cells were established by lentivirus-mediated gene transfection. The effects of ING5 overexpression on the proliferation of lung cancer A549 cells were observed by cell proliferation assay and clonogenic assay. The effects of WSTF on the migration and invasion of lung cancer cells were observed by Trans-well migration assay and invasion assay. Results: Western blot showed that the WSTF protein level in A549-WSTF cells was significantly higher than that in control A549 cells (P = 0.0004). WSTF overexpression significantly promoted the proliferation of lung cancer cells (P value of 1-4 days were 0.002, 0.0004, 0.0002 and 3.21 × 10-5, respectively) and clonality (P = 0.004). WSTF overexpression also significantly promoted lung cancer The cell migration from trans-well cells to the lower cells showed OD570 values of 0.626 ± 0.013 (A549-WSTF) and 0.322 ± 0.010 (A549-control), respectively, P = 2.37 × 10-5. WSTF also promoted lung cancer cells to wear Matrigel permeate into the lower chamber with OD570 values of 0.600 ± 0.027 (A549-WSTF) and 0.333 ± 0.017 (A549-control), respectively, with P = 0.0004. Conclusion: WSTF can promote the proliferation and invasion ability of lung cancer cells and play a role in cancer promotion.