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
- Wencheng Yu
- Liyun Mi
- Feifei Wang
Affiliations: Department of Pulmonary and Critical Care Medicine, The Affiliated Hospital of Qingdao University, Qingdao, Shandong 266003, P.R. China, Department of Respiratory Medicine, Qingdao Chest Hospital, Qingdao, Shandong 266043, P.R. China
- Published online on: December 5, 2019 https://doi.org/10.3892/mmr.2019.10863
Copyright: © Yu
et al. This is an open access article distributed under the
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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.