该研究探讨了IQGAP1(IQ domain GTPase-activating protein 1)对非小细胞肺癌(nonsmall cell lung cancer,NSCLC)细胞增殖的影响及其对ERK信号通路的调节作用。将内源性IQGAP1低表达的A549细胞中分为空白组、空载组和IQGAP1过表达组;将内源性IQGAP1高表达的H1299细胞中分为空白组、阴性对照si RNA组和IQGAP1 si RNA组;采用ERK1/2磷酸化抑制剂U0126处理上述两株细胞。MTT法检测细胞增殖能力,Western blot法检测ERK1/2和p-ERK1/2蛋白质水平。结果显示,在A549细胞中,过表达IQGAP1能促进细胞增殖并促进ERK1/2磷酸化;在H1299中,敲低IQGAP1表达能够抑制细胞增殖并下调ERK1/2磷酸化水平。用U0126处理后能抑制IQGAP1对细胞增殖的促进作用。研究结果表明,IQGAP1可通过ERK信号通路促进体外非小细胞肺癌细胞增殖。 This study investigated the effect of IQGAP1 on the proliferation of nonsmall cell lung cancer (NSCLC) cells and its regulation of ERK signaling pathway. The A549 cells with low expression of endogenous IQGAP1 were divided into blank group, empty vector group and IQGAP1 overexpression group. H1299 cells with high expression of endogenous IQGAP1 were divided into blank group, negative control si RNA group and IQGAP1 si RNA The two strains were treated with ERK1 / 2 phosphorylation inhibitor U0126. The cell proliferation was detected by MTT assay. The protein levels of ERK1 / 2 and p-ERK1 / 2 were detected by Western blot. The results showed that in A549 cells, overexpression of IQGAP1 can promote cell proliferation and promote ERK1 / 2 phosphorylation; in H1299, knockdown of IQGAP1 expression can inhibit cell proliferation and down-regulate ERK1 / 2 phosphorylation. U0126 treatment can inhibit the promotion of IQGAP1 cell proliferation. The results show that IQGAP1 can promote the proliferation of non-small cell lung cancer cells in vitro through ERK signaling pathway.