Department of Thoracic Surgery, First Hospital of China Medical University, Shenyang, Liaoning 110001, P.R. China.
Oncol Rep. 2020 May;43(5):1437-1450. doi: 10.3892/or.2020.7526. Epub 2020 Feb 28.
Lung adenocarcinoma is one of the most common malignant tumors worldwide. Although efforts have been made to clarify its pathology, the underlying molecular mechanisms of lung adenocarcinoma are still not clear. The microarray datasets GSE75037, GSE63459 and GSE32863 were downloaded from the Gene Expression Omnibus (GEO) database to identify biomarkers for effective lung adenocarcinoma diagnosis and therapy. The differentially expressed genes (DEGs) were identified by GEO2R, and function enrichment analyses were conducted using the Kyoto Encyclopedia of Genes and Genomes (KEGG) and Gene Ontology (GO). The STRING database and Cytoscape software were used to construct and analyze the protein‑protein interaction network (PPI). We identified 376 DEGs, consisting of 83 upregulated genes and 293 downregulated genes. Functional and pathway enrichment showed that the DEGs were mainly focused on regulation of cell proliferation, the transforming growth factor β receptor signaling pathway, cell adhesion, biological adhesion, and responses to hormone stimulus. Sixteen hub genes were identified and biological process analysis showed that these 16 hub genes were mainly involved in the M phase, cell cycle phases, the mitotic cell cycle, and nuclear division. We further confirmed the two genes with the highest node degree, DNA topoisomerase IIα (TOP2A) and aurora kinase A (AURKA), in lung adenocarcinoma cell lines and human samples. Both these genes were upregulated and associated with larger tumor size. Upregulation of AURKA in particular, was associated with lymphatic metastasis. In summary, identification of the DEGs and hub genes in our research enables us to elaborate the molecular mechanisms underlying the genesis and progression of lung adenocarcinoma and identify potential targets for the diagnosis and treatment of lung adenocarcinoma.
肺腺癌是全球最常见的恶性肿瘤之一。尽管已经努力阐明其病理学,但肺腺癌的潜在分子机制仍不清楚。从基因表达综合数据库(GEO)下载了 GSE75037、GSE63459 和 GSE32863 微阵列数据集,以鉴定用于有效肺腺癌诊断和治疗的生物标志物。通过 GEO2R 鉴定差异表达基因(DEGs),并使用京都基因与基因组百科全书(KEGG)和基因本体论(GO)进行功能富集分析。使用 STRING 数据库和 Cytoscape 软件构建和分析蛋白质-蛋白质相互作用网络(PPI)。我们鉴定了 376 个 DEGs,包括 83 个上调基因和 293 个下调基因。功能和途径富集表明,DEGs 主要集中在细胞增殖调节、转化生长因子 β 受体信号通路、细胞黏附、生物黏附以及对激素刺激的反应。鉴定了 16 个枢纽基因,生物过程分析表明,这 16 个枢纽基因主要参与 M 期、细胞周期各阶段、有丝分裂细胞周期和核分裂。我们进一步证实了在肺腺癌细胞系和人类样本中具有最高节点度的两个基因,即 DNA 拓扑异构酶 IIα(TOP2A)和极光激酶 A(AURKA)。这两个基因均上调,与更大的肿瘤大小有关。AURKA 的上调尤其与淋巴转移有关。总之,我们的研究中 DEGs 和枢纽基因的鉴定使我们能够详细阐述肺腺癌发生和发展的分子机制,并确定用于肺腺癌诊断和治疗的潜在靶标。