ArticleMolecular medicine reports2020
Effect of the alteration of Tribbles homologue 3 expression on epithelial‑mesenchymal transition of transforming growth factor β1‑induced mouse alveolar epithelial cells through the Wnt/β‑catenin signaling pathway.
Article in Molecular medicine reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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3 citing papers in PubMed, 3 citations in OpenAlex.
- MDA5 protein mediating persistent ER stress/unfolded protein response contributes to endothelial-mesenchymal-transition of lung microvascular endothelial cell in dermatomyositis.Cell communication and signaling : CCS · 2025Article
- TGF‑β1: Gentlemanly orchestrator in idiopathic pulmonary fibrosis (Review).International journal of molecular medicine · 2021Review
- Molecular Pathogenesis of Pulmonary Fibrosis, with Focus on Pathways Related to TGF-β and the Ubiquitin-Proteasome Pathway.International journal of molecular sciences · 2021Review
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The aims of the present study were to elucidate the regulatory effect of exogenous Tribbles homologue 3 (TRB3) expression on the Wnt/β‑catenin signaling pathway and epithelial‑mesenchymal transition (EMT) in transforming growth factor‑β1 (TGF‑β1)‑induced mouse alveolar epithelial cells (MLE‑12) and investigate the underlying regulatory mechanisms. TRB3 expression was upregulated and downregulated using gene overexpression and RNA interference techniques, respectively. TGF‑β1‑stimulated MLE‑12 cells were examined for EMT and activation condition of the Wnt/β‑catenin signaling pathway using Cell Counting Kit‑8, flow cytometry, western blotting, reverse transcription‑quantitative PCR, ELISA and immunofluorescence techniques. During TGF‑β1‑induced EMT, TRB3 expression was found to be significantly upregulated (P<0.05). In the TRB3 overexpression group, upregulated expression of β‑catenin and EMT‑related genes and proteins was observed (P<0.05), and an increase in fibrosis‑related factors in the cell culture supernatant was detected (P<0.05); however, the results were the opposite in the TRB3 downregulated group (P<0.05). TRB3 may be involved in the regulation of EMT in TGF‑β1‑induced MLE‑12 cells through the Wnt/β‑catenin signaling pathway.
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