Differential Expression of lncRNA CASC2 in the Serum of Childhood Asthma and Its Role in Airway Smooth Muscle Cells Proliferation and Migration

Purpose: Asthma is a common chronic disease in children. Abnormal expression of lncRNAs can be used as biomarkers for early diagnosis of asthma. The present study aimed to explore the expression change and clinical value of lncRNA CASC2 in asthma, and further investigate its potential mechanism. Patients and Methods: Seventy asthma children and 66 healthy controls were recruited. Levels of mRNAs were detected using qRT-PCR. Receiver operating characteristic (ROC) curves were drawn for diagnostic value evaluation. Asthma cell models were established using PDGF-BB in Human airway smooth muscle cells (ASMCs). Levels of Th1/Th2 related cytokines were detected using ELISA. Lipofectamine 3000 was used for cell transfection. The target relationship was verified using luciferase activity assay. Results: CASC2 was at a low level in asthma children in comparison with the healthy controls. Serum CASC2 can distinguish healthy individuals from asthma children. Overexpression of CASC2 inhibited PDGF-BB induced cell proliferation and migration. CASC2 upregulation inhibited the release of Th2 related cytokines (IL-4 and IL-10), but promoted the release of Th1-related cytokine (IFN-gamma). In PDGF-BB treated ASMCs, the reduced expression of contractile phenotype marker (alpha-SMA) was detected, but the trend was reversed by CASC2 upregulation. LncRNA CASC2 serves as a ceRNA of miR-31-5p, overexpression of miR-31-5p reversed the influence of CASC2 on asthma in vitro. Conclusion: Serum CASC2 can distinguish healthy individuals from asthma children. CASC2 may be involved in childhood asthma through inhibiting ASMCs proliferation, migration and inflammation via sponging miR-31-5p.

Automated summary

This study explores the expression change and clinical value of lncRNA CASC2 in asthma. The results show that serum CASC2 can distinguish healthy individuals from asthma children. CASC2 may be involved in childhood asthma by inhibiting ASMCs proliferation, migration, and inflammation via sponging miR-31-5p.