Cofilin-1基因在人胶质瘤细胞侵袭、迁移、粘附中的分子机制

摘要

[目的]探讨Cofilin-1基因在人胶质瘤细胞侵袭、迁移及细胞粘附中的分子机制.[方法]采用 RNAi技术干扰人胶质瘤细胞系 SHG-44细胞中 Cofilin-1基因的表达.Real-time PCR及 Western blot检测验证 Cofi-lin-1干扰效果;划痕实验检测细胞迁移能力;Transwell小室实验检测细胞侵袭能力;粘附作用实验检测细胞粘附能力;Western blot检测细胞中 ICAM-1及胞质和胞核中 NF-κB p65蛋白水平的表达.[结果]RNAi干扰可降低SHG-44细胞中 Cofilin-1的表达水平;Cofilin-1表达干扰抑制 SHG-44细胞迁移、侵袭及粘附能力,降低细胞中ICAM-1的表达,下调胞核中 NF-κB p65的表达水平.[结论]干扰Cofilin-1表达能够抑制胶质瘤细胞的迁移、侵袭及粘附,可能通过调节 NF-κB通路活化发挥作用,Cofilin-1可能成为胶质瘤的潜在治疗靶点.%[Objective]To investigate the effects and possible molecular mechanisms of interfering Cofilin-1 gene ex-pression on the invasion,migration and cell adhesion in human glioma cells.[Methods]The RNAi technique was used to interfere with the expression of Cofilin-1 gene in human glioma cell line SHG-44.The interference effect of Cofilin-1 was verified by Real-time PCR and Western blot.Scratch assay was used to detect cell migration ability.Transwell chamber assay was used to detect cell invasion ability.Adhesion experiment was used to detect cell adhesion ability.The expression of ICAM-1 and NF-κB p65 protein in cytoplasm and nucleus were detected by Western blot.[Results]RNAi interference successfully inhibited the expression of Cofilin-1 in SHG-44 cells.Interference of Cofilin-1 expression inhibited the migra-tion,invasion and adhesion in SHG-44 cells,decreased the expression of ICAM-1 and the expression of NF-κB p65 in nu-cleus.[Conclusion]Interference of Cofilin-1 expression can inhibit the migration,invasion and adhesion in glioma cells, and may play a role by regulating the activation of NF-κB pathway.Cofilin-1 may be a potential therapeutic target for glio-mas.