Postoperative delirium (POD) is clinically associated with a variety of adverse outcomes. The incidence of POD in patients undergoing radical resection of lung cancer is about 5% to 16%, higher than that in patients undergoing other surgeries. However, the molecular mechanisms that specifically lead to POD after radical resection of lung cancer have not been fully elucidated. Gene expression profile datasets of lung cancer (GSE31210) and POD (GSE163943) were downloaded from the Gene Expression Omnibus database. The weighted gene co-expression network analysis (WGCNA) was used to screen key model genes. Differentially expressed genes between disease and control groups were selected. Function enrichment analysis was applied to reveal various biological processes of genes. The hub factors were further selected by protein–protein interaction network, and potential therapeutic drugs were screened using molecular docking. A total of 28 differentially expressed co-expression key module genes shared by lung cancer and POD were obtained. These genes were involved in Fanconi anemia pathway, glycosaminoglycan degradation, and pentose phosphate pathway. A predicted protein–protein interaction network was constructed, which contained 7 proteins. CDC20 (cell division cycle protein 20) had a higher degree. Molecular docking revealed that the drug ergotamine had the lowest docking binding energy with the target protein. Fanconi anemia pathway, glycosaminoglycan degradation and pentose phosphate pathway may play a key role in the pathogenesis of POD after lung cancer surgery via. Ergotamine may serve as a candidate drug for lung cancer-related POD.
Qian et al. (Fri,) studied this question.