MicroRNA-148b inhibits proliferation and the epithelial-mesenchymal transition and increases radiosensitivity in non-small cell lung carcinomas by regulating ROCK1.

Non-small cell lung cancer (NSCLC) accounts for ~80% of all types of lung cancer, which has the highest morbidity and mortality of all types of cancer worldwide. It is important to identify novel biomarkers and the molecular mechanism of NSCLC to improve current treatments of NSCLC. The present study aimed to investigate the effect of miR-148b expression on the proliferation, epithelial-mesenchymal transition (EMT) and radiosensitivity of NSCLC cells. It was demonstrated that miR-148b expression was significantly decreased in NSCLC tissues and cell lines. A549 cells were then transfected with a miR-148b mimic and a miR-148b inhibitor. Transfection with the miR-148b mimic decreased proliferation whereas transfection with the miR-148b inhibitor increased the proliferation of A549 cells. Additionally, the miR-148b mimic increased E-cadherin expression and decreased N-cadherin and vimentin expression. By contrast, transfection with the miR-148b inhibitor decreased E-cadherin expression and increased N-cadherin and vimentin expression. Irradiation-induced cell death was significantly promoted by the miR-148b mimic but inhibited by the miR-148b inhibitor. The miR-148b mimic significantly decreased the expression of Rho-associated protein kinase 1 (ROCK1) and it was demonstrated that overexpression of ROCK1 significantly inhibited the effects of miR-148b on cell proliferation, the EMT and irradiation-induced cell death. Therefore, the current study revealed that miR-148b inhibited NSCLC cell proliferation and the EMT, and increased the radiosensitivity of NSCLC cells by inhibiting ROCK1 expression. Therefore, miR-148b/ROCK1 signaling may be a novel therapeutic target to inhibit the growth of NSCLC cells and enhance the effects of radiotherapy to treat patients with NSCLC.