Objective To investigate the role of collagen triple helical repeat 1 (CTHRC1) in the process of epithelial-mesenchymal transition (EMT) in chronic obstructive pulmonary disease (COPD) by regulating the non-canonical Wnt signaling pathway.

Methods The expression levels of CTHRC1 in lung tissue samples from COPD patients and healthy controls were investigated using the GSE130928 and GSE151052 databases. The expression levels of CTHRC1 and EMT markers were detected by western blotting in COPD mouse models and cellular models by exposure to cigarette smoke (CS) or cigarette smoke extract (CSE).

Results In GSE130928 and GSE151052, the expression level of CTHRC1 in lung tissue of COPD patients was significantly higher than that of control group (P ＜ 0.01). Compared with the control group, the protein level of CTHRC1 in the CS group was significantly up-regulated (P ＜ 0.05). After 12 weeks of exposure to incense CS, the expression of E-cadherin was down-regulated in mouse lung tissue (P ＜ 0.05), whereas the expression of vimentin was up-regulated (P ＜ 0.05). The CSE exposure resulted in the decreasing of E-cadherin expression in HBE cells (P ＜ 0.01), while the expression of vimentin increased (P ＜ 0.01). The CTHRC1 knockdown significantly reversed the changes in E-cadherin and vimentin in CSE-stimulated HBE cells, which could alleviate CSE-induced EMT by downregulating the β-catenin pathway, and the changes in EMT-inducing transcriptional factor β-catenin, p-β-catenin caused by CTHRC1 knockdown could be partly reversed by the activator Lithium chloride (LiCl).

Conclusions CTHRC1 can mediate the development of EMT in COPD progression through Wnt/β-catenin signaling.