Inhibition of long non-coding RNA NEAT1 suppressed the epithelial mesenchymal transition through the miR-204-5p/Six1 axis in asthma.

Abstract

Asthma, a prevalent chronic respiratory condition, is characterized by airway remodeling. Long non-coding RNA (lncRNA) NEAT1 has been demonstrated to participate in airway fibrosis. Furthermore, the miR-204-5p/Six1 axis significantly influences epithelial mesenchymal transition (EMT). However, the function of NEAT1/miR-204-5p/Six1 in asthmatic EMT remains unclear. This study intends to elucidate the function of NEAT1/miR-204-5p/Six1 axis in asthmatic EMT. TGF-β1 was used to induce the EMT model in BEAS-2B cells. Immunofluorescence and western blot were executed to verify the establishment of the EMT model. NEAT1, miR-204-5p, and Six1 expression levels were evaluated using RT-qPCR. The role of NEAT1 in EMT in vitro was explored by CCK8 assays and flow cytometry. The luciferase reporter assay was performed to validate the interaction between NEAT1 and miR-204-5p/Six1. NEAT1 expression was increased during EMT. Functional experiments showed that the knockdown of NEAT1 suppressed cell proliferation and promoted cell apoptosis in vitro. Furthermore, inhibition of NEAT1 decreased the expression of N-cadherin, vimentin, and α-SMA and increased the expression of E-cadherin. Mechanistically, NEAT1 was identified as a sponge for miR-204-5p, and Six1 was found to be a direct target of miR-204-5p. Down-regulation of NEAT1 reduced the Six1 expression via targeting miR-204-5p to inhibit the process of EMT in asthma. This study may provide new insight to reveal the underlying mechanisms of asthma.