ArticleLaboratory investigation; a journal of technical methods and pathology2021
miR-184 targets TP63 to block idiopathic pulmonary fibrosis by inhibiting proliferation and epithelial-mesenchymal transition of airway epithelial cells.
Article in Laboratory investigation; a journal of technical methods and pathology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.
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Who cites it
8 citing papers in PubMed, 1 synthesis or guideline pooled it, 21 citations in OpenAlex.
- The dual role of miR-184 in cancer: a systematic review of context-dependent regulation.Molecular biology reports · 2025Pooled it
- TP63 regulates pyroptosis via NF-κB/NLRP3/caspase-1 signaling in interstitial cystitis: insights from single-cell sequencing.Open medicine (Warsaw, Poland) · 2026Article
- Role of epigenetics in corneal health and disease.Progress in retinal and eye research · 2025Review
- MiR-125b-5p alleviates pulmonary fibrosis by inhibiting TGFβ1-mediated epithelial-mesenchymal transition via targeting BAK1.Respiratory research · 2024Article
- circGRHPR inhibits aberrant epithelial-mesenchymal transformation progression of lung epithelial cells associated with idiopathic pulmonary fibrosis.Cell biology and toxicology · 2024Article
- microRNA-184 in the landscape of human malignancies: a review to roles and clinical significance.Cell death discovery · 2023Review
- Downregulation of microRNA‑423‑5p suppresses TGF‑β1‑induced EMT by targeting FOXP4 in airway fibrosis.Molecular medicine reports · 2022Article
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
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. TP63 knockdown in BEAS-2B and A549 cell lines significantly attenuated above-described TGF-β1-induced fibrotic changes. miR-184 targeted TP63 3'-UTR to inhibit Tp63 expression. miR-184 overexpression within BEAS-2B and A549 cell lines also attenuated TGF-β1-induced fibrotic changes. miR-184 overexpression attenuated bleomycin-induced pulmonary fibrosis in mice. Moreover, TP63 overexpression aggravated TGF-β1-stimulated fibrotic alterations within BEAS-2B and A549 cells and significantly reversed the effects of miR-184 overexpression, indicating miR-184 relieves TGF-β1-stimulated fibrotic alterations within BEAS-2B and A549 cells by targeting TP63, while TP63 overexpression reversed miR-184 cellular functions. In conclusion, the miR-184/TP63 axis modulates the TGF-β1-induced fibrotic alterations in epithelial cell lines and bleomycin-induced pulmonary fibrosis in mice. Therefore, these results confirm that the miR-184/TP63 axis is involved in IPF progression.
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