PRR11调节肺癌细胞系A549侵袭迁移的分子机制研究

Silencing PRR11 inhibits the migration and invasion of lung cancer A549 cells

摘要:

目的：PRR11（proline rich protein 11）是近年来发现的一个肿瘤相关基因，前期研究结果显示其高表达对于肺癌等恶性肿瘤细胞的侵袭迁移具有重要作用，本研究为了更进一步研究其促进肺癌细胞侵袭转移的分子机制。方法：综合利用siRNA敲减、划痕及迁移实验、Western blot及免疫荧光等方法分析人肺癌细胞系A549沉默PRR11表达后细胞侵袭迁移能力下降的分子机制。结果：PRR11沉默后，划痕及Transwell实验结果表明，PRR11沉默明显减弱了A549细胞运动、侵袭及迁移能力。进一步定量qRT-PCR及Western blot检测发现，PRR11稳定沉默导致上皮细胞标志分子E-cadherin明显上调、而EMT上游关键转录因子Twist1及间质细胞标志分子N-cadherin表达下调，另外免疫荧光染色结果同样显示Twist1及N-cadherin下调明显。结论：肺癌细胞系A549中PRR11可能通过调节Twist1等EMT关键分子的表达在细胞侵袭转移过程中起关键作用，为进一步探索PRR11在肺癌中的作用机制奠定了基础。

Abstract:

Objective：To further investigate the molecular mechanism that proline rich protein 11（PRR11） implicates in migration and invasion in lung cancercells. Methods：PRR11 was down-regulated using siRNA in lung cancer cell A549. The migration and inva－sion abilities was detected using wound healing，Transwell，siRNA，and EMT relative proteins was analyzed by Western blot and IF assay. Results：Our results demonstrated that PRR11 depletion significantly inhibited the migration and invasion abilities in A549 cells using wound healing and Transwell. Furthermore，the expression levels of the Twist1 and N-cadherin were down-regulated in PRR11 depletion significantly than that of control using qRT-PCR，Western blot and IF. Conclusion：PRR11 depletion significantly inhibites the migration and invasion abilities in lung cancer cell line. It suggests that high-level expression of PRR11 enhance the migration and invasion activities in lung cancer，but the molecular mechanism is worth for further study.