目的：研究 IQ 结构域三磷酸鸟苷合酶－激活蛋白1（IQGAP1）在口腔鳞状细胞癌（OSCC）组织中的表达，探讨其对肿瘤细胞增殖和侵袭的影响及其作用机制。方法：免疫印迹和荧光定量 PCR 检测 IQGAP1在癌组织和癌旁组织中的表达水平；利用脂质体转染法将重组质粒 pcDNA3．1-IQGAP1转入人口腔鳞状细胞癌细胞系 SCC-4，并用 Akt 抑制剂预处理，免疫印迹检测 Akt 磷酸化水平、MTT 法和 Transwell 侵袭实验分别测定细胞增殖和侵袭能力的变化。结果：IQGAP1蛋白和 mRNA 表达量显著高于癌旁组织（P ＜0．05），重组质粒转染后，SCC-4细胞中 IQGAP1表达量明显增加，细胞的增殖能力和侵袭能力增强（P＜0．05）。IQGAP1过表达后细胞中 p Akt 水平明显升高；当用 Akt 抑制剂处理后，IQGAP1诱导的 p Akt 的水平明显降低，细胞增殖和侵袭能力降低（P ＜0．05）。结论：IQGAP1在 OSCC 组织中高表达，可能通过调节 Akt 通路的活化来介导癌细胞的增殖和侵袭能力。%Objective:To study the expression of IQ motif containing GTPase activating protein 1 (IQGAP1 )in oral squamous cell cancer(OSCC)tissue,and to explore the effects of IQGAP1 on cell proliferation and invasion as well as its underlying mechanism. Methods:Expression levels of IQGAP1 in tumor and adjacent normal tissues were examined by western blot and RT-PCR.OSCC cell line SCC-4 cells was transfected with the recombinant plasmid-pcDNA3.1 -IQGAP1 by lipofectamine,and then treated with an Akt in-hibitor.The phosphorylation of Akt,cell proliferation and invasion were detected by western blot,MTT assay and Transwell invasion as-say respectively.Results:Protein and mRNA expression levels of IQGAP1 were higher in cancer tissue than in adjacent normal tissue (P <0.05).Transfection of pcDNA3.1 -IQGAP1 increased IQGAP1 expression,enhanced the capability of cell proliferation and inva-sion (P <0.05),increased p Akt level in the cells.Preconditioning with an Akt inhibitor reduced p Akt level.Furthermore,silencing Akt pathway blocked the increase of cell proliferation and invasion induced by IQGAP1 overexpression(P <0.05).Conclusion:IQ-GAP1 overexprission can mediate the ability of proliferation and invasion of OSCC cells by regulating the activation of Akt pathway.
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