miR-128-3p inhibits EMT and invasion of lung carcinoma cells by targeting SIRT1

Objective: To figure out the function and mechanism of miR-128-3p in the progression of lung carcinoma. Methods: miR-128-3p and SIRT1 expression in lung carcinoma cells A549, H460, H1650, SK-MES-1 and normal lung epithelial cell BEAS-2B were measured with the help of qRT-PCR and Western blot. miR-128-3p over-expression and SIRT1 inhibitory vector were transfected into A549 and H1650 cells, respectively. CCK-8, transwell and flow cytometry were applied to observe cell proliferation, invasion and apoptosis. Changes of epithelial-mesenchymal transition (EMT) markers N-cadherin, Vimentin and E-cadherin were detected. The relationship between miR-128-3p and SIRT1 was determined by means of dual luciferase reporter. Results: miR-128-3p was reduced in the four types of lung carcinoma cells, while SIRT1 was up-regulated. After A549 and H1650 were treated with miR-128-3p overexpression or SIRT1 inhibition, both proliferation and invasion ability of the two were inhibited and their apoptosis increased, and E-cadherin was elevated, while N-cadherin and Vimentin were reduced in cells. The dual luciferase reporter identified a targeted regulatory correlation between miR-128-3p and SIRT1. Conclusion: miR-128-3p can inhibit EMT and invasion of lung carcinoma cells via targeting SIRT1.