细胞黏附分子ICAM-1的表达在肿瘤组织中普遍上调，临床数据分析发现ICAM-1的表达水平与肺癌患者的预后呈负相关，但ICAM-1在肺癌发生发展中的功能目前尚不明确。本项目将研究ICAM-1对于肺癌细胞生存和凋亡的作用及机制。目前，我们已发现与正常肺上皮细胞相比，ICAM-1在多种肺癌细胞系中高表达，敲低肺癌细胞中的ICAM-1表达会引起肺癌细胞凋亡。因为肿瘤可以分泌表达多种ICAM-1结合蛋白，我们将深入研究ICAM-1多种结合蛋白的表达及其对ICAM-1下游信号的影响，发现激活肿瘤细胞胞内凋亡信号的ICAM-1及其结合蛋白的相互作用，揭示该相互作用的分子基础及其对于胞内凋亡信号的调控机制。最终，在肺癌小鼠模型中验证ICAM-1信号通路在肿瘤发生发展中的作用，并通过干预ICAM-1通路抑制肿瘤。本项目研究将揭示ICAM-1为肺癌细胞提供存活信号的新机制，为肺癌的治疗提供了潜在的分子靶标。

Cell adhesion molecule ICAM-1 is significantly up-regulated in various types of cancers, which is associated with poor prognosis in patients with lung cancer. However, its role in lung cancer has not been clearly elucidated. Herein, the aim of this study is to investigate the contribution of ICAM-1 to lung cancer cell survival. We have preciously found that ICAM-1 was up-regulated in lung cancer compared with normal lung epithelial cells. Knockdown of ICAM-1 resulted in apoptosis of lung cancer cells. Next, we plan to further investigate the interactions of ICAM-1 and its binding ligands, and its downstream signaling in regulating lung cancer cell apoptosis. In addition, we will use mouse model to investigate the biological functions of ICAM-1 in lung cancer progression. This study will reveal a novel mechanism of ICAM-1 in promoting cancer cell survival and its therapeutic prospects in lung cancer.