Aim: The study aims to pinpoint hub genes and investigate their functions in order to gain insightful understandings of lung adenocarcinoma (LUAD). Methods: Bioinformatic approaches were adopted to investigate genes in databases including Gene Expression Omnibus, WebGestalt, STRING and Cytoscape, GEPIA2, Oncomine, Human Protein Atlas, TIMER2.0, UALCAN, cBioPortal, TargetScanHuman, OncomiR, ENCORI, Kaplan-Meier plotter, UCSC Xena, European Molecular Biology Laboratory - European Bioinformatics Institute Single Cell Expression Atlas and CancerSEA. Results: Five hub genes were ascertained. CHEK1 was overexpressed in a range of cancers, including LUAD. Promoter methylation, amplification and miRNA regulation might trigger CHEK1 upregulation, signaling poor prognosis. CHEK1 with its coexpressed genes were enriched in the cell cycle pathway. Intratumor heterogeneity of CHEK1 expression could be observed. Cell clusters with CHEK1 expression were more prone to metastasis and epithelial-to-mesenchymal transition. Conclusion:CHEK1 might potentially act as a prognostic biomarker for LUAD.
Keywords: CHEK1; bioinformatics; hub genes; lung adenocarcinoma; prognosis.
Lay abstract Lung adenocarcinoma is the most common type of lung cancer. Many genes are thought to be linked to the development of cancers. We looked at key genes in lung adenocarcinoma by analyzing public databases. Five key genes, including CHEK1, were found. The amount of CHEK1 was higher in lung adenocarcinoma than in normal lung cells. The presence of a large amount of CHEK1 was linked to poor survival in people with lung adenocarcinoma. Also, CHEK1 was mainly expressed in some specific tumor cell clusters rather than in all tumor cell clusters. The clusters with CHEK1 expression were more cancerous compared with other clusters. Overall, CHEK1 might be a potential marker to predict survival in people with lung adenocarcinoma.