白血病抑制因子通过JAK1/STAT3信号通路调控非小细胞肺癌细胞活性

Leukemia inhibitory factor regulating cell activity of non-small cell lung cancer through the JAK1/STAT3 signaling pathway

目的:探讨白血病抑制因子(LIF)对非小细胞肺癌(NSCLC)的潜在作用及其机制。方法:采用免疫组织化学法、荧光定量PCR法、Western blot法检测LIF在NSCLC患者癌旁组织和肿瘤组织中的表达情况;采用CCK-8法和Transwell小室法检测LIF对肿瘤细胞A549细胞的增殖和侵袭作用的影响;Western blot检测JAK1/STAT3信号通路蛋白表达情况。结果:LIF在NSCLC的癌组织中的表达显著高于癌旁组织(P<0.01),经LIF共孵育后,肿瘤细胞的增殖和侵袭能力均明显增强(P<0.05);Western blot显示肿瘤细胞中JAK1、STAT3磷酸化水平明显提高(P<0.05)。结论:LIF在NSCLC中表达增加,可能通过JAK1/STAT3信号通路介导LIF的增加,并增强肿瘤细胞的增殖和侵袭能力。

Objective:To investigate the effect of leukemia inhibitor factor(LIF)on non-small cell lung cancer(NSCLC)and its possible mechanism.Methods:Immunohistochemical,fluorescent quantitative PCR and Western blot were used to detect the expression of LIF in non-small cell lung cancer patients paracancer tissue and tumor tissue.The effect of LIF on the proliferation and invasion of tumor cell A549 cells was detected by CCK-8 and Transwell chamber.Western blot was used to detect the expression of JAK1/STAT3 signaling pathway protein.Results:The expression of LIF in cancer tissues of NSCLC was significantly higher than that of paracancer tissues(P<0.01).After co-incubation with LIF,the proliferation and invasion ability of tumor cells were significantly enhanced(P<0.05).Western blot showed that tumor cells JAK1 and STAT3 phosphorylation levels were significantly increased(P<0.05).Conclusion:LIF expression is increased in NSCLC.The increased LIF can enhance the proliferation and invasion ability of tumor cells,which may be mediated through the JAK1/STAT3 signaling pathway.