MicroRNA-181a promotes epithelial-mesenchymal transition in esophageal squamous cell carcinoma via the TGF-β/Smad pathway

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.