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pmid:37887075
Identification of Hub Genes in Idiopathic Pulmonary Fibrosis and Their Association with Lung Cancer by Bioinformatics Analysis.
Juan Manuel Velázquez-Enríquez · Itayetzi Reyes-Avendaño · Jovito Cesar Santos-Álvarez · Edilburga Reyes-Jiménez · Verónica Rocío Vásquez-Garzón · Rafael Baltiérrez-Hoyos
Advances in respiratory medicine · 2023 doi:10.3390/arm91050032
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Experiment
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Complete file
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However, the etiology and pathogenesis of IPF have not yet been fully described. Moreover, lung cancer is a significant complication of IPF and is associated with increased mortality. Nevertheless, identifying common genes involved in developing IPF and its progression to lung cancer remains an unmet need. The present study aimed to identify hub genes related to the development of IPF by meta-analysis. In addition, we analyzed their expression and their relationship with patients' progression in lung cancer.\nMETHOD: Microarray datasets GSE24206, GSE21369, GSE110147, GSE72073, and GSE32539 were downloaded from Gene Expression Omnibus (GEO). Next, we conducted a series of bioinformatics analysis to explore possible hub genes in IPF and evaluated the expression of hub genes in lung cancer and their relationship with the progression of different stages of cancer.\nRESULTS: A total of 1888 differentially expressed genes (DEGs) were identified, including 1105 upregulated and 783 downregulated genes. The 10 hub genes that exhibited a high degree of connectivity from the PPI network were identified. Analysis of the KEGG pathways showed that hub genes correlate with pathways such as the ECM-receptor interaction. Finally, we found that these hub genes are expressed in lung cancer and are associated with the progression of different stages of lung cancer.\nCONCLUSIONS: Based on the integration of GEO microarray datasets, the present study identified DEGs and hub genes that could play an essential role in the pathogenesis of IPF and its association with the development of lung cancer in these patients, which could be considered potential diagnostic biomarkers or therapeutic targets for the disease.", "claims": [{"id": "claim-method", "statement": "We used the effect size combination method, specifically the random effects model (REM) and default settings for the integration of differential gene expression.", "kind": "methodological", "target": null, "evidence": [{"asset": "source:pmid:37887075", "locator": "sections[5] \"2.3. 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