Objective: To explore the effect and mechanism of miR-149-5p in apoptosis

epithelial-mesenchymal transition (EMT) and microtubule formation in human oral squamous cell carcinoma (OSCC). Methods: miR-149-5p mimic (mimic) and pcDNA-FGF5 (FGF5) were singly or co-transfected with CAL-27 cell line

and RT-PCR and Western blot were used to detected the expression FGF5; dual luciferase report test was used to verify the targeting relationship between miR-149-5p and FGF5. The apoptosis rate was detected by flow cytometry

and the expression of Bax/Bcl-2 protein was detected by Western blot. The morphological transformation of EMT cells was observed

and the expression of epithelial and interstitial markers E-cadherin (E-cad) and N-cadherin (N-cad) in CAL-27 cells was detected by Western blot. The microtubule-like formation ability of CAL-27 cells was detected by tube-forming test

and the expression of vascular endothelial growth factor (VEGF) was detected by Western blot. Results: miR-149-5p mimic could significantly inhibit the expression of FGF5 in CAL-27 cells (P=0.000); miR-149-5p mimic could significantly reduce the luciferase activity of FGF5 wild plasmid (P=0.000); miR-149-5p mimic increased the apoptosis rate of CAL-27 cells and Bax/Bcl-2 ratio significantly (P=0.000)

and reversed the increase of apoptosis rate (P=0.014) and Bax/Bcl-2 ratio caused by FGF5 overexpression (P=0.000). miR-149-5p mimic inhibited the EMT transformation on cell morphology from round to spindle shape

and reversely transformed the mesenchymal-like cell morphology caused by FGF5 overexpression. miR-149-5p mimic up-regulated the expression of E-cad in CAL-27 cells (P=0.000)

down-regulated the expression of N-cad (P=0.0009)

reversed the down-regulated expression of E-cad (P=0.020) and the up-regulated expression of N-cad (P=0.000) caused by FGF5 overexpression. miR-149-5p overexpression significantly inhibited the formation of microtubule nodules in CAL-27 cells (P=0.002)

reduced the expression level of VEGF protein (P=0.000)

and reversed the upregulation of VEGF expression caused by overexpression of FGF5 (P=0.000). Conclusion: miR-149-5p can inhibit EMT and microtubules formation and apoptosis promotion of OSCC cells. The mechanism of action is related to the targeted inhibition of FGF5 expression.