Abstract：Objective: To observe the effect of entinoslate on the proliferation, migration and invasion of oral squamous cell carcinoma cell line WSU-HN6, and to explore the potential relationship between its mechanism and miR-103a-3p / mechanically sensitive ion channel protein (PIEZO1) pathway. Methods: WSU-HN6 cells were treated with entenolate (0.0, 0.5, 1.0, 2.0, 4.0 μmol/L) for 24, 48 and 72 hours. The optimum concentration was 2.0 μmol/L and the optimum treatment time was 48 hours. The WSU-HN6 cells were transfected by liposome method. Cell proliferation rate was detected by cell counting kit (CCK8), and cell migration and invasion were detected by Transwell test. Western blot (WB) was used to detect E-cadherin, N-cadherin and PIEZO1 protein; the expression of miR-103a-3p and PIEZO1 was detected by real-time fluorescence quantitative polymerase chain reaction (RT-qPCR);the binding ability of miR-103a-3p to PIEZO1 was detected by double luciferase reporter gene experiment. Results: Entinostat (0.5, 1.0, 2.0, 4.0 μmol/L) inhibited the proliferation of WSU-HN6 cells in a concentration and time-dependent manner. The optimal concentration was 2.0 μmol/L for 48 hours. Compared with the 0.0 μmol/L group, the amount of cell migration and invasion significantly decreased, the expression of E-cadherin significantly increased, the expression of N-cadherin significantly decreased, the expression of miR-103a-3p significantly increased, and the expression of PIEZO1 significantly decreased in the 2.0 μmol/L group (P<0.05). After inhibiting miR-103a-3p, the cell proliferation rate, migration and invasion were all significantly reduced, the expression of E-cadherin was significantly reduced, and the expression of N-cadherin was significantly increased, and the overexpression of PIEZO1 had similar functions. The double luciferase report experiment showed that miR-103a-3p targeted and negatively regulated the mRNA and protein expression of PIEZO1. Knockdown of PIEZO1 significantly enhanced the inhibitory effect of entinostat on cell proliferation, migration and invasion, and weakened the promoting effect of inhibiting miR-103a-3p on cell proliferation, migration and invasion. Conclusion: Entinostat inhibits the proliferation, migration and invasion of oral squamous cell carcinoma cells. The potential mechanism of this anticancer effect may be related to the up regulation of miR-103a-3p and the inhibition of PIEZO1.
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2022, Vol. 28 
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