The silencing of lnc-NONHSAT071210 suppresses the proliferation, fibrosis, migration, and invasion of TGFβ1-treated lung epithelial cells

BACKGROUND: Pulmonary fibrosis, which is a frequent manifestation of connective tissue disease (CTD), is a leading cause of morbidity and mortality. However, the role of long non-coding ribonucleic acids (lncRNAs) in CTD-associated pulmonary fibrosis requires clarification. This study sought to examine the effects of lnc-NONHSAT071210 on the phenotypes of transforming growth factor β1 (TGFβ1)-treated lung epithelial cells. METHODS: The GeneChip was used to identify differentially expressed lncRNAs in CTD-associated pulmonary fibrosis patients. After lnc-NONHSAT071210 was knocked down in the TGFβ1-challenged lung epithelial cells, cell viability, cell cycle, migration, and invasion were estimated by Cell Counting Kit-8 assays, a flow cytometry analysis, wound-healing assays, and transwell assays, respectively. The expression and levels of the fibrosis-associated factors were examined by enzyme-linked immunosorbent assays, RT-qPCR, and western blots. RESULTS: The expression of the top 7 most significantly upregulated lncRNAs in the CTD-associated pulmonary fibrosis patients was depicted in a heat map and examined by reverse transcription-quantitative polymerase chain reaction (RT-qPCR). The results showed that the expression of lnc-NONHSAT071210 was significantly increased in the tissues of the CTD-associated pulmonary fibrosis patients (P<0.001). The silencing of Lnc-NONHSAT071210 suppressed proliferation, migration, and invasion in the TGFβ1-exposed alveolar epithelial cells (P<0.001). CONCLUSIONS: Thus, lnc-NONHSAT071210 expression was increased in the tissues of the CTD-associated pulmonary fibrosis patients and TGFβ1-treated lung epithelial cells, and TGFβ1-induced lung epithelial cell injury was alleviated by impeding the expression of lnc-NONHSAT071210.