IL-10是一种具有肿瘤免疫双向调控作用的抗炎因子，其在肺癌发病中的作用及机制尚不明确，miRNA被认为在炎症和肿瘤之间起着重要的调控作用。我们在前期研究中发现IL-10与非小细胞肺癌(NSCLC)的发病风险密切相关，以IL-10刺激NSCLC细胞时，miR-125b表达水平显著下调，进一步的细胞功能学实验发现在NSCLC细胞中，miR-125b抑制了IL-10的促癌作用。后续的基因芯片及IPA分析发现，下调miR-125b后，IGF-1信号通路显著激活。由此推测，IL-10/miR-125b/IGF-1信号轴可能在NSCLC发生发展中起着重要的作用。本课题中，我们将在完善前期功能学实验的基础上，着重分析IL-10/miR-125调控IGF-1信号通路，促进NSCLC发生发展的具体机制，并在整体动物水平进行验证。为NSCLC发病机制及诊治策略研究提供新的依据和思路。

IL-10 is an anti-inflammatory factor with bi-directional regulation of tumor immunity. However, the role and mechanism of IL-10 in lung cancer is still not clear. MicroRNA plays an important role in the development of inflammation related cancer. In our previous study, IL-10 was found significantly associated with the risk of Non-small Cell Lung Cancer (NSCLC). Meanwhile, the expression of miR-125b in NSCLC cell line was dramatically decreased when stimulated by IL-10. The results of cell functional experiments showed that miR-125b inhibited the tumor promoting effects of IL-10 in NSCLC. Then, microarray and IPA analysis showed that IGF-1 signaling pathway was significantly activated after we down-regulated the expression of miR-125b. Thus, we speculated that IL-10/miR-125b/IGF-1 axis might play an important role in the initiation and development of NSCLC. In the present study, we will firstly finish the functional experiments, and then focus on the mechanism of IL-10/miR-125 in regulating the IGF-1 signaling pathway. Finally, we will verify the function and mechanism of IL-10/miR-125b/IGF-1 axis in whole animal level. We hope our study could provide new evidence and ideas for the mechanism research and treatment strategy of NSCLC.