Antagonism Of Mir-21 Reverses Radiation-Induced Emt In Alveolar Epithelial Cells Via Pi3k/Akt Pathway

Radiation-induced lung injury (RILI) is a common complication after thoracic radiotherapy and epithelial-to-mesenchymal transition (EMT) an important change among this process. The aim of this study was to determine the role of miR-21 in radiation-induced EMT in alveolar epithelial type II cells RLE-6TN and explored the underlying molecular mechanism. The results showed that treating RLE-6TN cells with 8 Gy of X-ray promoted EMT and resulted in up-regulation of miR-21. Transfection of Rle-6TN cells with miR-21 inhibitor before IR caused an increase in expression of epithelial marker e-cadherin, as well as a decrease in the mesenchymal markers a-smooth muscle actin and vimentin. It indicated that downregulation of miR-21 in RLE-6TN cells inhibited the radiation-induced EMT. Moreover, miR-21 inhibitor decreased the progress of this EMT accompanied by a decrease of phosphorylated-Akt protein level. However, PI3K activator IGF-1 reversed the suppression of phosphorylated-Akt and promoted the radiation-induced EMT by miR-21 knockdown. In addition, we found a dose-dependent relationship between PI3K inhibitor LY294002 and radiation-induced EMT. In total, we concluded that antagonism of mir-21 reversed radiation-induced EMT in alveolar epithelial cells via PI3K/Akt pathway. This might be a much promising target in the cure the radiation-induced lung injury.