IQGAP1通过ERK信号通路促进非小细胞肺癌细胞增殖

IQGAP1 Promotes Cell Proliferation through ERK Pathway in Non-small Cell Lung Cancer

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 regulation of IQGAP1 on proliferation and ERK pathway in non- small cell lung cancer （NSCLC） cells. A549 cells, with low endogenous IQGAP1 expression, were treated with blank, Ad-GFP and Ad-GFP-IQGAP1, respectively. H1299 cells, with high endogenous IQGAP1 expression, were treated with blank, control siRNA and IQGAP1 siRNA, respectively. Then, it was followed by MTT assay analysis for cell proliferation and Western blot analysis for ERK protein level. In addition, the two cell lines were treated with U0126, an ERK1/2 phosphorylation inhibitor. The results indicated that IQGAP1 over expression promotes cell proliferation and up-regulate the p-ERK1/2 expression in A549 cells, while knock-down IQGAP1 results in the opposite scenario in H1299 cells. Meanwhile, U0126 treatment restrained the promotion of IQGAP1 on cell proliferation. These results suggested that IQGAP1 promotes cell proliferation through ERK pathway in NSCLC.