MiR-184 targets TP63 to block idiopathic pulmonary fibrosis by inhibiting proliferation and epithelial-mesenchymal transition of airway epithelial cells.

ABSTRACT: Epithelial-to-mesenchymal transition (EMT) of epithelium and airway epithelial cell proliferation disorder are key events in idiopathic pulmonary fibrosis (IPF) pathogenesis. During EMT, epithelial cell adhesion molecules (EpCAM, such as E-cadherin) are downregulated, cytokeratin cytoskeletal transforms into vimentin-based cytoskeleton, and the epithelial cells acquire mesenchymal morphology. In the present study, we show abnormal upregulation of tumor protein p63 (TP63) and downregulation of miR-184 in IPF. Transforming growth factor beta 1 (TGF-β1) stimulation of BEAS-2B and A549 cell lines significantly increased the protein levels of Tp63, alpha-smooth muscle actin (α-SMA), and vimentin, but decreased EpCAM protein levels, and promoted viability of both BEAS-2B and A549 cell lines. TP6

SUBMITTER: Li J 

PROVIDER: S-EPMC7815506 | biostudies-literature | 2021 Feb

REPOSITORIES: biostudies-literature