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

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。

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

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 thatof 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.