淋巴结转移是导致肺癌不良预后的一个主要因素。肌球蛋白轻链激酶（MYLK）是一种细胞骨架蛋白，已报道它在多种肿瘤的增殖和转移中发挥作用，但它在肺癌淋巴转移中的作用及其机制尚未阐明。前期工作中我们发现在肺癌淋巴转移患者肿瘤组织中MYLK mRNA、蛋白表达显著高于未转移组，且利用非标记定量蛋白质组学和磷酸化多肽段分析发现MYLK对糖代谢信号转导通路多个代谢酶有调控作用，这提示MYLK可能在肺癌淋巴结转移中发挥重要作用，其机制可能和糖代谢相关。本项目拟采用条件共培养和原位转移模型研究MYLK调控肺癌淋巴结转移的作用及其分子机制。首先，利用过表达和干扰MYLK明确肺癌细胞株A549和H460细胞转移能力的变化，以及验证明确MYLK 具体调控的下游信号通路，揭示MYLK调控非小细胞肺癌淋巴结转移的分子机制，这将为开发非小细胞肺癌淋巴结转移的新靶点奠定理论基础。

Lymphatic metastasis is one of the main factors for the lung cancer poor prognosis. MYLK (Myosin light chain kinase)is acytoskeletal protein that has been reported it to play the role in the proliferation and metastasis of a variety of tumors, but its role in lymphatic metastasis of lung cancer and its mechanism has not been elucidated.Preliminary work showed that the level of MYLK mRNA and protein expression in tumor tissues of patients withlung cancer lymphatic metastasis was significantly higher than that in the group without metastasis.By means of non labeling quantitative proteomics and phosphorylated polypeptide segment analysis ,it was found that MYLK could regulate several enzymes involved in carbohydrate metabolism, suggesting that MYLK may play an important role in lymph node metastasis of lung cancer and the possible mechanism was related to glucose metabolism.This Project aims to study the molecular mechanism of metastasis of lung cancer lymph node of MYLK regulation, by using the co-culture condition and Nude mice transplantation tumor model. Observing the metastatic phenotype of A549 and H460 cells of lung cancer cell line by over expression and silencing of MYLK. And screening and verifying the changes of genes and proteins in the model, finding out the MYLK specific regulation of the cytokines and downstream signaling pathways, to prove that MYLK is a key molecule in non small cell lung cancer lymph node metastasis, contribute to the inhibition of lung cancer metastasis of new therapeutic targets.