Open AccessMicroRNA‑181a promotes epithelial‑mesenchymal transition in esophageal squamous cell carcinoma via the TGF‑β/Smad pathway
Author(s) -
Renxin Xu,
Xuemei Zhou,
Yushan Li,
Li Ren,
Xin-Rong He
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.2021.11955
Subject(s) - epithelial–mesenchymal transition , vimentin , cancer research , microrna , smad , oncogene , transfection , cell growth , apoptosis , cell cycle , flow cytometry , biology , cell , cell migration , transforming growth factor , downregulation and upregulation , cell culture , immunohistochemistry , microbiology and biotechnology , immunology , biochemistry , genetics , gene
Esophageal squamous cell carcinoma (ESCC) is one of the most debilitating and invasive tumors. Although previous reports have demonstrated the critical role microRNA‑181a (miR‑181a) serves in the progression of ESCC, how miR‑181a induces epithelial‑mesenchymal transition (EMT) remains to be elucidated. In the present study, the expression profiles of TGF‑β1 and Smad4 proteins in 88 patients with ESCC and 21 adjacent non‑cancerous tissues were analyzed using immunohistochemistry. The expression of miR‑181a in ESCC cells (ECA109 and TE‑1) and HEEC was analyzed using reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR). The role of miR‑181a in ESCC was analyzed using miR‑181a mimics and inhibitor in the same system. Migration, proliferation and apoptosis of cells were assessed using wound‑healing assays and cell proliferation assays and flow cytometry, respectively. The expression levels of TGF‑β1 and Smad4 in ESCC cell lines transfected with miR‑181a mimics and inhibitor were measured using RT‑qPCR and western blotting. The expression of E‑cadherin and vimentin was also assessed following transfection. The findings demonstrated that expression of TGF‑β1 was upregulated, in contrast to Smad4 expression which was downregulated. Expression levels of Smad4 affected the prognosis of patients with ESCC. Higher expression of miR‑181a promoted migration and proliferation but inhibited apoptosis of ESCC cells. miR‑181a promoted EMT by modulating Smad4 expression in ESCC cells. Overall, these findings revealed that miR‑181a induced EMT in ESCC via the TGF‑β/Smad pathway in ESCC. Consequently, miR‑181a is a potential novel target against ESCC.