Clinical Significance and Potential Mechanism of miR-532-5p/CXCL1 Axis in Chronic Obstructive Pulmonary Disease

Chronic obstructive pulmonary disease (COPD) involves persistent airflow limitation and chronic inflammation. To define the clinical and mechanistic role of the miR-532-5p/CXCL1 axis in COPD, this study used bioinformatic analysis of the GEO dataset GSE70080 to identify miR-532-5p, which was significantly down-regulated in COPD. Multiple databases predicted CXCL1 as its potential target gene. The clinical study included 90 subjects (52 with COPD, 38 controls). We detected serum levels of miR-532-5p and CXCL1 mRNA using RT-qPCR and evaluated their diagnostic value through ROC curves and logistic regression. Inflammatory factors (TNF-α, IL-1β) and oxidative stress indicators (SOD, MDA) were measured by ELISA and colorimetry. A dual-luciferase reporter gene assay verified that miR-532-5p directly targets CXCL1. In BEAS-2B cells treated with cigarette smoke extract (CSE), we conducted functional recovery experiments by transfecting miR-532-5p mimics and CXCL1 over-expression vectors to explore their regulatory role in cell injury. The study found that the expression of miR-532-5p in the serum of COPD patients was down-regulated, and its level was correlated with the decline of lung function and the enhancement of inflammation. It also had a diagnostic value for COPD (AUC = 0.8229) and was an independent protective factor. Mechanistically, CXCL1 was confirmed to be a direct target of miR-532-5p; in the cell smoke injury model; miR-532-5p inhibited CXCL1 to alleviate inflammation and oxidative stress. This study identifies miR-532-5p as a potential protective factor in COPD that acts by targeting CXCL1 to mitigate inflammation and oxidative stress, suggesting its diagnostic and therapeutic relevance.