白血病抑制因子对非小细胞肺癌细胞增殖和侵袭的影响及其机制

目的 探讨非小细胞肺癌（NSCLC）中白血病抑制因子（leukemia inhibitory factor, LIF）对细胞增殖和侵袭的影响及其作用机制。方法 采用荧光定量PCR和Western blot检测LIF在人NSCLC组织和癌旁组织中的表达；应用重组LIF因子处理非小细胞肺癌细胞系A549和Z793, MTT技术检测重组LIF因子对细胞增殖的影响; Transwell实验检测重组LIF因子对细胞侵袭的影响；Western blot检测重组LIF因子对肿瘤细胞中AKT/mTOR信号通路的影响。结果 LIF在肺癌组织中的表达水平较正常癌旁组织显著上调（P=0.0078）。重组LIF处理A549和Z793细胞后，肿瘤细胞增殖较对照组明显增加（P<0.01）；肿瘤细胞的侵袭能力较对照组明显增强（P<0.01）；AKT蛋白的磷酸化水平明显增加，且其下游底物mTOR的表达显著上调。结论 LIF在非小细胞肺癌中表达上调，并通过激活AKT/mTOR信号通路促进非小细胞肺癌细胞的增殖和侵袭。

Effect of Leukemia Inhibitory Factor on Proliferation and Invasion of Non-small Cell Lung Cancer Cells and Related Mechanism

Objective To explore the influence of leukemia inhibitory factor(LIF) on the proliferation and invasion of non-small cell lung cancer(NSCLC) cells. Methods The expression of LIF in human NSCLC tissues and adjacent tissues were detected by fluorescent quantitative PCR and Western blot. After NSCLC cell lines A549 and Z793 were treated with recombinant LIF, we detected cell proliferation by MTT assay, cell invasion by Transwell assay, and ATK/mTOR pathway by Western blot. Results LIF expression was higher in lung cancer tissues than that in the matched adjacent tissues(P=0.0078). After A549 and Z793 cell lines were treated with recombinant LIF, the tumor cells showed a significantly higher proliferation rate and invasiveness in vitro than those in control group(P<0.01); moreover, the phosphorylated AKT level was significantly elevated and the expression of mammalian target of rapamycin(mTOR), the AKT downstream targets, was obviously up-regulated. Conclusion LIF expression is significantly increased in NSCLC cells. In addition, the ectopic expression of LIF promotes cell proliferation and invasion via activating AKT/mTOR pathway.