Nav1.6-RNAi通过AKT通路抑制口腔鳞癌细胞增殖作用研究

Nav1.6-RNAi inhibits the proliferation of oral squamous cell carcinoma cells through the AKT pathway

目的探讨Nav1.6-RNAi对口腔鳞状细胞癌细胞增殖作用的影响,并分析其可能相关机制。方法使用免疫组化、Western blot和qRT-PCR法检测电压门控钠通道Nav1.6在口腔鳞状细胞癌组织中的表达情况;将Nav1.6-RNAi转染到人舌鳞癌细胞株(CAL-27细胞)中,使用Western blot法检测Nav1.6、CyclinD1、C-myc、AKT及p-AKT的表达,并通过流式细胞仪检测细胞周期。结果免疫组化、Western blot和qRT-PCR结果证实Nav1.6在口腔鳞状细胞癌组织中表达高于口腔正常组织(P<0.05);Nav1.6-RNAi转染到CAL-27细胞中后,CyclinD1、C-myc、p-AKT蛋白表达降低(P<0.05),且S期细胞明显减少。结论电压门控钠通道Nav1.6可能通过AKT通路参与口腔鳞状细胞癌的增殖。

Objective To explore the biological effects of Nav1.6-RNAi on the proliferation of oral squamous cell carcinoma cell lines and analyze its possible regulatory mechanism.Methods Immunohistochemistry,Western blot and qRT-PCR were used to detect the expression of Nav1.6 in oral squamous cell carcinoma tissues.After Nav1.6-RNAi transfected into oral squamous cell carcinoma,Western blot was used to validate the expression of CyclinD1,C-myc,AKT and p-AKT.Cell cycle was also detected by flow cytometry.Results Immunohistochemistry,Western blot and qRT-PCR showed that the expression of Nav1.6 in oral squamous cell carcinoma tissues was significantly higher than that in normal oral tissues(P<0.05).After Nav1.6-RNAi transfected into oral squamous cell carcinoma,the expression of CyclinD1,C-myc and p-AKT protein significantly decreased compared with the control group(P<0.05),and the cells in S phase significantly reduced.Conclusion Voltage-gated sodium channel Nav1.6 can affect the proliferation of oral squamous cell carcinoma through the AKT pathway.