To explore the impact of mechanical injury on the growth of airway epithelial cells by simulating mechanical damage through mechanical scratches, and to investigate the role of the miR-766-3p/PNCK/m-TOR pathway in this process.

The airway epithelial cells were transfected with has-miR-766-3p mimics, inhibitors, and corresponding negative control(NC), and the airway epithelial cells were mechanically scratched to create a damage model; cell counting kit-8(CCK8) method was used to detect cell viability; hematoxylin-eosin staining(HE) staining analysis of cell morphology; Transwell method for detecting cell migration ability; Western blot(WB) was used to detect protein expression levels; Quantitative reverse transcription polymerase chain reaction(RT qPCR)was used to detect RNA expression levels.

After modeling, the hsa-miR-766-3p RNA expression of cells decreased (1.01 vs. 0.31), the invasion ability decreased (180 vs. 123), and the cell activity decreased (0.97 vs. 0.72). The differences were statistically significant (P<0.05). After cell modeling, overexpression of miR-766-3p decreased cell invasion ability (127 vs. 94.5) and cell activity (0.7 vs. 0.52). After inhibitory expression of miR-766-3p, cell invasion ability (118 vs. 217) and activity (0.69 vs. 0.87) increased. The differences were statistically significant (P<0.05). After inhibitory expression of miR-766-3p, the expression of Pregnancy-upregulated nonubiquitous calmodulin kinase(PNCK)(0.34 vs. 0.84) and mammalian Target of rapamycin(mTOR)(0.45 vs. 1.05) increased, and the difference was statistically significant (P<0.05).

Through in vitro cell studies, it is believed that mechanical injury can affect the expression of miR-766-3p, and miR-766-3p further influences the activity and migration ability of airway epithelial cells by affecting the expression of PNCK and mTOR.