Open AccessDownregulation of miR‑483‑5p inhibits TGF‑β1‑induced EMT by targeting RhoGDI1 in pulmonary fibrosis
Author(s) -
Guichuan Huang,
Jing Zhang,
Gang Qing,
Daishun Liu,
Xin Wang,
Yi Chen,
Yongchang Wu,
Yishi Li,
Shuliang Guo
Publication year - 2021
Publication title -
molecular medicine reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.727
H-Index - 56
eISSN - 1791-3004
pISSN - 1791-2997
DOI - 10.3892/mmr.2021.12177
Subject(s) - epithelial–mesenchymal transition , microrna , gene knockdown , cancer research , protein kinase b , downregulation and upregulation , transforming growth factor , pi3k/akt/mtor pathway , oncogene , biology , chemistry , transfection , signal transduction , microbiology and biotechnology , cell cycle , apoptosis , cell culture , gene , biochemistry , genetics
Transforming growth factor‑β1 (TGF‑β1)‑induced epithelial‑mesenchymal transition (EMT) serves a significant role in pulmonary fibrosis (PF). Increasing evidence indicates that microRNAs (miRNAs or miRs) contribute to PF pathogenesis via EMT regulation. However, the role of miR‑483‑5p in PF remains unclear. Therefore, the present study investigated the potential effect of miR‑483‑5p on TGF‑β1‑induced EMT in PF. It was found that the expression of miR‑483‑5p was upregulated in both PF tissue and A549 cells treated with TGF‑β1, whereas expression of Rho GDP dissociation inhibitor 1 (RhoGDI1) was downregulated. miR‑483‑5p mimic transfection promoted TGF‑β1‑induced EMT; by contrast, miR‑483‑5p inhibitor inhibited TGF‑β1‑induced EMT. Also, miR‑483‑5p mimic decreased RhoGDI1 expression, whereas miR‑483‑5p inhibitor increased RhoGDI1 expression. Furthermore, dual‑luciferase reporter gene assay indicated that miR‑483‑5p directly regulated RhoGDI1. Moreover, RhoGDI1 knockdown eliminated the inhibitory effect of the miR‑483‑5p inhibitor on TGF‑β1‑induced EMT via the Rac family small GTPase (Rac)1/PI3K/AKT pathway. In conclusion, these data indicated that miR‑483‑5p inhibition ameliorated TGF‑β1‑induced EMT by targeting RhoGDI1 via the Rac1/PI3K/Akt signaling pathway in PF, suggesting a potential role of miR‑483‑5p in the prevention and treatment of PF.