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Abstract
Background
Asthma, a prevalent chronic respiratory disorder, remains enigmatic, notwithstanding considerable advancements in our comprehension. Continuous efforts are crucial for discovering novel molecular targets and gaining a comprehensive understanding of its pathogenesis.
Materials and methods
In this study, we analyzed gene expression data from 212 individuals, including asthma patients and healthy controls, to identify 267 differentially expressed genes, among which C1orf64 and C7orf26 emerged as potential key genes in asthma pathogenesis. Various bioinformatics tools, including differential gene expression analysis, pathway enrichment, drug target prediction, and single-cell analysis, were employed to explore the potential roles of the genes.
Results
Quantitative PCR demonstrated differential expression of C1orf64 and C7orf26 in the asthmatic airway epithelial tissue, implying their potential involvement in asthma pathogenesis. GSEA enrichment analysis revealed significant enrichment of these genes in signaling pathways associated with asthma progression, such as ABC transporters, cell cycle, CAMs, DNA replication, and the Notch signaling pathway. Drug target prediction, based on upregulated and downregulated differential expression, highlighted potential asthma treatments, including Tyrphostin-AG-126, Cephalin, Verrucarin-a, and Emetine. The selection of these drugs was based on their significance in the analysis and their established anti-inflammatory and antiviral invasion properties. Utilizing Seurat and Celldex packages for single-cell sequencing analysis unveiled disease-specific gene expression patterns and cell types. Expression of C1orf64 and C7orf26 in T cells, NK cells, and B cells, instrumental in promoting hallmark features of asthma, was observed, suggesting their potential influence on asthma development and progression.
Conclusion
This study uncovers novel genetic aspects of asthma, highlighting potential therapeutic pathways. It exemplifies the power of integrative bioinformatics in decoding complex disease patterns. However, these findings require further validation, and the precise roles of C1orf64 and C7orf26 in asthma warrant additional investigation to validate their therapeutic potential.
Ethical approval
This study was conducted in accordance with the guidelines of the Ministry of Science and Technology of China and relevant national regulations, and was approved by the Ethics Committee of the Second Affiliated Hospital of Guangxi Medical University.
Authors contributions
Zhengzhao Li and Yun Ling designed the experiments. Lianshan Guo and Enhao Huang conducted data mining analysis and molecular experimental validation. Tongting Wang supported the data analysis. Lianshan Guo and Enhao Huang wrote the manuscript. All authors discussed and revised the manuscript.
Disclosure statement
No potential conflict of interest was reported by the author(s).
Data availability statement
The data that supports the findings of this study, including any relevant details needed to reproduce the published results, are available from the corresponding author upon reasonable request.