The objective was to explore the function of gene differential expressions between lung cancer tissues and the interaction between the relevant encoded proteins, thereby analyzing the important genes closely related to lung cancer. A total of 120 samples from the GEO database (including two groups, i.e., 60 lung cancer in situ specimens and 60 normal specimens) were taken as the research objects, which were submitted to the analysis of signaling pathway, biological function enrichment, and protein interactions to reveal the molecular driving mechanism of lung cancer. Results: A total of 875 differentially expressed genes were obtained, including 291 up-regulated genes and 584 down-regulated genes. The up-regulated genes were mainly involved in biological processes such as protein metabolism, protein hydrolysis, mitosis, and cell division. Down-regulated genes were mainly involved in neutrophil chemotaxis, inflammatory response, immune response, and angiogenesis. The protein expression of high expression genes and low expression genes in patients were higher than those in the control group. The protein corresponding to the high expression gene was highly expressed in the patient group. Meanwhile, the proteins corresponding to the low expression genes were also expressed in the patient group, which showed that although the proteins corresponding to the low expression genes were low in the patients, they were still the target genes related to lung cancer. In conclusion, the molecular driving mechanism in lung cancer was mainly related to protein metabolism, proteolysis, mitosis, and cell division. It was found that TOP2A, CCNB1, CCNA2, CDK1, and TTK might be the critical target genes of lung cancer.

目的是探讨肺癌组织间基因差异表达的功能及相关编码蛋白之间的相互作用，从而分析与肺癌密切相关的重要基因。GEO数据库共120个样本（包括两组，即60个肺癌就地标本和60个正常标本）作为研究对象，进行信号通路、生物学功能富集和蛋白质相互作用分析，以揭示肺癌的分子驱动机制。结果：共获得875个差异表达基因，其中上调基因291个，下调基因584个。上调基因主要参与蛋白质代谢、蛋白质水解、有丝分裂和细胞分裂等生物学过程。下调基因主要参与中性粒细胞趋化、炎症反应、免疫反应和血管生成。患者高表达基因和低表达基因的蛋白表达量均高于对照组。高表达基因对应的蛋白质在患者组中高表达。同时，低表达基因对应的蛋白在患者组中也有表达，说明低表达基因对应的蛋白虽然在患者体内低表达，但仍是肺癌相关的靶基因。综上所述，肺癌的分子驱动机制主要与蛋白质代谢、蛋白水解、有丝分裂和细胞分裂有关。发现TOP2A、CCNB1、CCNA2、CDK1和TTK可能是肺癌的关键靶基因。它们仍然是肺癌相关的靶基因。综上所述，肺癌的分子驱动机制主要与蛋白质代谢、蛋白水解、有丝分裂和细胞分裂有关。发现TOP2A、CCNB1、CCNA2、CDK1和TTK可能是肺癌的关键靶基因。它们仍然是肺癌相关的靶基因。综上所述，肺癌的分子驱动机制主要与蛋白质代谢、蛋白水解、有丝分裂和细胞分裂有关。发现TOP2A、CCNB1、CCNA2、CDK1和TTK可能是肺癌的关键靶基因。