NSCLC高死亡率与侵袭转移密切相关，受转移相关分子的调控。研究表明蛋白激酶STK24可调控细胞迁移、增殖、凋亡和糖代谢等生理病理过程，但其在NSCLC转移中的确切作用和机制尚不明确。我们首先通过生物信息学分析和临床样本组化检测发现STK24的表达与NSCLC的发生和转移密切相关；进一步利用乌拉坦诱导肺癌模型发现STK24促进肺肿瘤发生发展；体外细胞实验显示其可能机制为STK24磷酸化Akt调控EMT相关蛋白的表达从而促进肿瘤转移且依赖STK24激酶活性。本课题拟在此研究基础上，利用体内外实验进一步确定STK24在肺癌转移中的作用，明确STK24所调控的Akt磷酸化位点，及其他新的调控方式和靶点；同时扩大临床样本研究明确STK24的表达与NSCLC转移和预后相关性。本项目的完成有望阐明STK24磷酸化Akt方式及促进肺癌转移的新机制，为临床提供预后评价和潜在治疗靶点。

The high mortality of NSCLC is closely related to invasion and metastasis which regulated by the metastasis associated genes. Studies have shown that protein kinase STK24 regulated physiological and pathological processes such as cell migration, proliferation, apoptosis and glucose metabolism, however its function and mechanism in NSCLC metastasis is still unclear. First of all, we found that the expression of STK24 was closely related to the occurrence and metastasis of NSCLC through bioinformatics analysis and clinical sample histochemistry.Then using urethane-induced lung cancer model we found that STK24 promoted lung tumor metastasis; in vitro cell experiments showed that the possible mechanism was STK24 phosphoric acid. Akt regulated the expression of EMT-related proteins to promote tumor metastasis which was dependent on STK24 kinase site activity. Based on this research,we will further investigate the functions of STK24 in the lung cancer metastasis in vivo and in vitro, clarify the Akt phosphorylation site regulated by STK24 and other new regulatory methods and targets. At the same time, expand the clinical sample study to confirm the expression of STK24 is associated with NSCLC metastasis and prognosis. The completion of this project is expected to clarify the new mechanism of STK24 phosphorylation of Akt and promote lung cancer metastasis, and provide prognostic evaluation and potential therapeutic targets for the clinic.