LncRNA UCA1 regulates silicosis-related lung epithelial cell-to-mesenchymal transition through competitive adsorption of miR-204-5p

The main clinical manifestations are pulmonary fibrosis, silicosis, is one of the most common types of pneumoconiosis, and its pathogenesis is still unclear. The proliferation and transdifferentiation of fibroblasts are considered to be the key link leading to pulmonary fibrosis. Type II alveolar epithelial cells can be transformed into lung fibroblasts through epithelial-mesenchymal transition (EMT) to promote lung fibrosis. Involved in the EMT process of a variety of cancers, lncRNA UCA1 (UCA1) has been shown to competitively adsorb miR-204-5p, and play an effect on the downstream target gene E-box binding zinc finger protein 1 (ZEB1), thereby promoting EMT to facilitate the invasion and migration of cancer cells. This is an important potential intervention target that affects the process of EMT, but it has not been reported in the study of EMT related to silicosis. Therefore, this study established a SiO2 dust-treated mouse silicosis model and an in vitro EMT model of A549 cells to observe the changes and effects of UCA1 and miR-204-5p, and intervene on the two respectively. The results showed that the EMT process existed in the aforementioned models, while UCA1 was upregulated in the in vitro model. Double luciferase reporter assay demonstrated the targeted binding of UCA1 and miR-204-5p. Silencing UCA1 can up-regulate the expression of miR-204-5p and reduce the level of ZEB1, thus inhibiting EMT process, while intervention of miR-204-5p can change the level of ZEB1 and regulate EMT. Therefore, UCA1 may release its target gene ZEB1 through competitive adsorption of miR-204-5p to regulate EMT process.

Automated summary

This study observed the changes and effects of UCA1 and miR-204-5p in silica-induced mouse silicosis model and in vitro EMT model of A549 cells. It was found that both models showed the presence of EMT process, and UCA1 was upregulated in the in vitro model. Silencing UCA1 inhibited EMT process, while intervention of miR-204-5p regulated EMT.