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Background  Pulmonary fibrosis is a serious clinical fatal disease. Epithelial–mesenchymal transition (EMT) and lncRNA NEAT1 have been implied in its development and progression.    Objective  To study the role of lncRNA NEAT1 in the progression of fibrosis in human pulmonary epithelial cells (BEAS-2B). Specifically, BEAS-2B was transfected with NEAT1 and miR-29c, EMT and cell proliferation were measured and the expression level of relevant genes was determined by Western blot.    Result  Results showed that NEAT1 promotes fibrosis and proliferation of BEAS-2B cells via the up-regulation of α-SMA, Vimentin, Snail and proliferation-related genes including Cyclin D1 and Cyclin E; miR-29c is a target gene of NEAT1 and through which NEAT1 regulates EMT and expression of proliferation-related genes.    Conclusion  This study investigated the mechanism of pulmonary fibrosis progression by elucidating the role of NEAT1/miR-29c in the fibrosis and proliferation of BEAS-2B cells, thus providing a basis for the new therapeutic targets of pulmonary fibrosis.

The role and mechanism of lncRNA NEAT1 in the fibrosis of pulmonary epithelial cell