Unlocking TB-COPD Pathogenesis: A Biotechnological Approach Targeting the PI3K/Akt Pathway

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Dai Jin; Li Zheng; Jing Jing; Xu Dan; Wang Jing; Li Fengsen

مرکز اطلاعات علمی Scientific Information Database (SID) - Trusted Source for Research and Academic Resources

Journal Paper

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Journal: Iranian Journal of Biotechnology Year:621 | Volume: | Issue: Page(s): 42-59

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Title

Unlocking TB-COPD Pathogenesis: A Biotechnological Approach Targeting the PI3K/Akt Pathway

Author(s)

Keywords

Biotechnology

PI3K/Akt signaling

Tuberculosis

Chronic Obstructive Pulmonary Disease

WGCNA

Molecular Pathway Analysis

Abstract

Background: Tuberculosis (TB)-associated Chronic Obstructive Pulmonary Disease (COPD) represents a significant global health challenge, yet its underlying molecular mechanisms remain poorly understood. The PI3K/Akt signaling pathway is implicated in inflammatory responses and cellular survival, suggesting its potential role in TB-COPD pathogenesis.Objective: This study integrates computational and experimental Biotechnology approaches to identify key molecular mechanisms linking TB and COPD, with a focus on the PI3K/Akt signaling pathway.Methods: Weighted gene co-expression network analysis (WGCNA) was applied to two publicly available gene expression datasets (GSE42057, GSE83456) to identify differentially expressed genes and critical co-expression modules. Functional enrichment analysis (GO/KEGG) was performed to assess pathway involvement. Experimentally, a Mycobacterium Tuberculosis-infected bronchial epithelial cell model (16HBE) was established, and the PI3K/Akt inhibitor LY294002 was utilized to evaluate its effects on apoptosis, proliferation, and epithelial-mesenchymal transition (EMT) markers.Results: WGCNA identified a key module significantly enriched in PI3K/Akt signaling. Experimental validation demonstrated that LY294002 treatment significantly improved cell survival (p < 0.05), reduced apoptosis, and restored epithelial integrity, as indicated by increased E-Cadherin and decreased N-Cadherin expression. Furthermore, LY294002 suppressed PI3K/Akt mRNA expression and phosphorylation (p < 0.05), confirming pathway inhibition.Conclusion: This study provides a novel biotechnological perspective on the role of PI3K/Akt signaling in TB-COPD, highlighting its potential as a therapeutic target. The integrative use of bioinformatics and experimental validation strengthens our understanding of molecular pathogenesis, paving the way for precision medicine strategies in respiratory disease management.

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