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Xiao Chen,1,2 Jie Yao,1 Meng-Yu Zhang,1 Rui Li,1 Xiao Liu,1 Yi-Qing Qu1 1Department of Pulmonary and Critical Care Medicine, Qilu Hospital of Shandong University, Jinan, People’s Republic of China; 2Department of Respiratory Medicine, Tai’an City Central Hospital, Tai’an, People’s Republic of ChinaCorrespondence: Yi-Qing Qu, Department of Pulmonary and Critical Care Medicine, Qilu Hospital of Shandong University, Wenhuaxi Road 107#, Jinan, 250012, People’s Republic of China, Tel +86 531 8216 9335, Fax +86 531 8296 7544, Email quyiqing@sdu.edu.cnPurpose: Non-small cell lung cancer (NSCLC) is currently a problem in the clinic and in society. Tumor-related macrophages (TAMs) in the tumor microenvironment (TME) play a vital role in the development of NSCLC.Patients and Methods: Bioinformatics was used to analyze the role of Indoleamine 2,3-dioxygenase 1 (IDO1) in NSCLC and the correlation of its expression with CD163 expression. The expression of CD163 and IDO1 was measured by immunohistochemistry, and their colocalization was assessed by immunofluorescence. M2 macrophage polarization was induced, and a coculture model of NSCLC cells and macrophages was established.Results: Bioinformatics analysis showed that IDO1 promoted the metastasis and differentiation of NSCLC and inhibited DNA repair. Moreover, the expression of IDO1 was positively correlated with CD163 expression. We discovered that IDO1 expression was related to M2 macrophage differentiation. In vitro, we showed that increased IDO1 expression promoted the invasion, proliferation, and metastasis of NSCLC cells.Conclusion: In conclusion, we determined that IDO1 can regulate the M2 polarization of TAMs and promote the progression of NSCLC, which provides partial theoretical evidence for the use of IDO1 inhibitors in the treatment of NSCLC.Keywords: IDO1, NSCLC, M2 macrophage, TAM, bioinformatics

Jie Yang,1,2 Meng-Yu Zhang,1 Yi-Ming Du,2 Xiu-Li Ji,3 Yi-Qing Qu1 1Department of Pulmonary and Critical Care Medicine, Qilu Hospital of Shandong University, Shandong Key Laboratory of Infectious Respiratory Diseases, Jinan, People’s Republic of China; 2Department of Gerontology, The First Affiliated Hospital of Shandong First Medical University & Shandong Provincial Qianfoshan Hospital, Jinan, People’s Republic of China; 3Department of Pulmonary Disease, Jinan Traditional Chinese Medicine Hospital, Jinan, People’s Republic of ChinaCorrespondence: Yi-Qing Qu, Department of Pulmonary and Critical Care Medicine, Qilu Hospital of Shandong University; Shandong Key Laboratory of Infectious Respiratory Diseases, Wenhuaxi Road 107#, Jinan, 250012, People’s Republic of China, Tel +86 531 8216 9335, Fax +86 531 8296 7544, Email quyiqing@sdu.edu.cnPurpose: Cellular senescence participates in the occurrence and development of chronic obstructive pulmonary disease (COPD). This study aimed to identify senescence-related hub genes and explore effective diagnostic markers and therapeutic targets for COPD.Methods: The microarray data from the GSE38974 dataset was downloaded from the Gene Expression Omnibus (GEO) database. The overlapping genes between genes from the GSE38974 dataset and CellAge database were considered differentially expressed senescence-related genes (DESRGs). Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses were performed using R software. Protein-protein interaction (PPI), miRNA-mRNA network, and competitive endogenous RNA (ceRNA) network were constructed and visualized by Cytoscape software. GSE100281 and GSE103174 datasets were employed to validate the expression and diagnostic value of hub genes. Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) was used to measure the mRNA levels of hub genes in peripheral blood mononuclear cells (PBMCs) from COPD and control samples.Results: A

Yi-Can Yang,1 Meng-Yu Zhang,1 Jian-Yu Liu,1 Yuan-Yuan Jiang,2 Xiu-Li Ji,3 Yi-Qing Qu2 1Department of Pulmonary and Critical Care Medicine, Qilu Hospital, Cheeloo College of Medicine, Shandong University; Shandong Key Laboratory of Infectious Respiratory Diseases, Jinan, People’s Republic of China; 2Department of Pulmonary and Critical Care Medicine, Qilu Hospital of Shandong University; Shandong Key Laboratory of Infectious Respiratory Diseases, Jinan, People’s Republic of China; 3Department of Pulmonary Disease, Jinan Traditional Chinese Medicine Hospital, Jinan, People’s Republic of ChinaCorrespondence: Yi-Qing Qu, Department of Pulmonary and Critical Care Medicine, Qilu Hospital, Shandong University, Shandong Key Laboratory of Infectious Respiratory Diseases, Wenhuaxi Road 107#, Jinan, 250012, People’s Republic of China, Tel +86 531 8216 9335, Fax +86 531 8296 7544, Email quyiqing@sdu.edu.cnPurpose: Ferroptosis and immune infiltration are involved in the pathogenesis of chronic obstructive pulmonary disease (COPD). We aim to identify ferroptosis-related hub genes and analyze their association with immune infiltration in COPD through bioinformatics methods.Materials and Methods: The mRNA microarray data of GSE38974 were downloaded from Gene Expression Omnibus to obtain differentially expressed genes (DEGs). The DEGs were intersected with ferroptosis-related genes (FRGs) from FerrDb to obtain differentially expressed FRGs. GO and KEGG enrichment and protein–protein interaction (PPI) analyses of differentially expressed FRGs were conducted in R software and STRING database. The key module and hub genes were screened by Cytoscape software. MiRNAs, transcription factors and signal molecules were predicted in miRNet and NetworkAnalyst. The disease correlation in the Comparative Toxicomics Database (CTD) and the receiver operating characteristic (ROC) curves of hub genes were analyzed. Immune infiltration was evaluated by CIBERSORT algorithm. Spearman correlat

Zhuang-E Shi,1 Meng-Yu Zhang,1 Jian-Yu Liu,1 Wen-Di Zhang,1 Dong-Mei Hu,1 Qing-Xiang Wang,1 Xiu-Li Ji,2 Yuan-Yuan Jiang,3 Yi-Qing Qu3 1Department of Pulmonary and Critical Care Medicine, Qilu Hospital, Cheeloo College of Medicine, Shandong University, Shandong Key Laboratory of Infectious Respiratory Diseases, Jinan, People’s Republic of China; 2Department of Pulmonary Disease, Jinan Traditional Chinese Medicine Hospital, Jinan, People’s Republic of China; 3Department of Pulmonary and Critical Care Medicine, Qilu Hospital of Shandong University, Shandong Key Laboratory of Infectious Respiratory Diseases, Jinan, People’s Republic of ChinaCorrespondence: Yi-Qing Qu, Department of pulmonary and Critical Care Medicine, Qilu Hospital of Shandong University, Shandong Key Laboratory of Infectious Respiratory Diseases, Jinan, People’s Republic of China, Tel +86 531 8216 9335, Fax +86 531 8296 7544, Email quyiqing@sdu.edu.cnPurpose: Chronic obstructive pulmonary disease (COPD) is a predominant cause of mortality worldwide. Autophagy, which depends on a lysosomal degradation pathway, plays an essential role in the occurrence of COPD. The aim of our study was to identify the potential function of autophagy and construct a BCL2-related competing endogenous RNA (ceRNA) network that induces autophagy in COPD.Methods: Blood sample data from GSE31568, GSE24709, and GSE61741 were collected from the Gene Expression Omnibus (GEO) database. Differentially expressed miRNAs in COPD and controls were identified via GEO2R. Transcription factors were obtained from FunRich. DIANA, miRDB, miRTarBase, and TargetScan were used to predict target genes of miRNAs. Autophagy genes were collected from the Human Autophagy Database (HADb). The GSE151052 dataset was used to identify autophagy-related differentially expressed genes in tissues. Functional enrichment and protein–protein interaction (PPI) network analyses were conducted via Metascape and the STRING network. Spearman correlation a