肺癌是世界范围内最常见的恶性肿瘤之一，每年新发病例和死亡病例都超过100 万。中国人群90%的不吸烟和65%的吸烟肺腺癌患者肿瘤有EGFR,HER2,ALK,KRAS,ROS1 或RET 基因突变中的一种,这些突变都有对应的靶向药物，部分已经在临床上取得很好的疗效。但肺腺癌总体上有35%-50%的病例没有已知的致癌基因改变，肺鳞癌已知的致癌基因改变相对更少，这部分患者目前没有机会接受靶向治疗。在前期研究中，我们发现抑癌基因ARHGA24在肺癌组织中表达明显降低，ARHGA24基因抑制有望作为新的致癌基因改变并成为新的治疗靶点。本课题以高通量测序和生物信息学筛选为基础，通过临床样本验证和分析确定肺癌的候选抑癌基因ARHGAP24，并将在体外实验和体内实验两个层面上探讨ARHGAP24基因在肺癌发生和发展、侵袭、转移等生物学行为中的作用及相关机制。

Lung cancer is one of the most common malignant tumors with more than 1 million diagnoses and deaths per year worldwide. Lung cancers harboring specific driver mutations are sensitive to targeted drugs, which benefits lung cancer patients. Previous study showed that 90% of lung adenocarcinoma patients from Chinese never smokers and 65% smoker patients harbored a driver mutation involving EGFR, HER2, ALK, KRAS, ROS1 or RET. All these known driver mutations have corresponding targeted drugs, some of them(Gefitinib, Erlotinib and Crizotinib) have shown significant benefit for patients harboring specific mutations. However, about 35%-50% of unselected lung adenocarcinomas and most lung squamous cell carcinomas from all comers (smokers and never smokers) do not harbor a knowndriver mutation. So far, we have found the low expression of suppressor gene ARHGAP 24 in lung cancer.In this study,through vivo and vitro experiment we will further explore the function and mechanism of ARHGAP24 gene in the genesis, development, invasion and metastasis in lung cancer.