摘要
目的 :利用舌癌细胞系HN4,探讨蛋白激酶C(protein kinase C,PKC)、P120-连环蛋白(P120-catenin,P120ctn)和E-钙黏蛋白(E-cadherin,E-cad)在口腔鳞癌中的相互关系及其在肿瘤细胞侵袭和转移中的作用机制。方法:采用质粒p GFP-V-RS-P120ctn sh RNA转染HN4,使HN4中P120ctn的表达显著降低,再使用星孢菌素(staurosporine,STS)抑制PKC的表达,进行PKC、P120ctn和E-cad m RNA和蛋白水平的检测;通过Transwell细胞侵袭及细胞迁移试验等方法,检测PKC被抑制前、后肿瘤细胞迁移和侵袭能力的变化。采用SPSS18.0软件包对数据进行统计学分析。结果:当PKC被STS抑制时,HN4/sh P120ctn细胞中P120ctn的表达显著升高,E-cad的表达也随之升高,肿瘤细胞的迁移和侵袭能力显著降低(P均<0.05)。结论:PKC可能参与了P120ctn和E-cad表达的调节,与细胞黏附的调控有关,进而在HN4细胞的迁移和侵袭过程中发挥作用。
PURPOSE: By using HN4 cells, the correlation among protein kinase C(PKC), P120-catenin(P120ctn) and E-cadherin(E-cad) was investigated, and the role of them in migration and invasion of oral squamous-cell cancer(OSCC)was evaluated. METHODS: Plasmid p GFP-V-RS-P120 ctn sh RNA was used to transfect HN4 cells to significantly reduce the expression of P120 ctn and PKC inhibitor staurosporine(STS) was added. m RNA and protein expression of PKC,P120 ctn and E-cad were tested and Transwell cell invasion and cell migration assay was used to test the invasion and migration capacity before and after PKC inhibition. Statistical analysis was performed using SPSS 18.0 software package.RESULTS: When PKC was inhibited by STS, the expression of P120 ctn and E-cad in OSCC cells were increased and the migration and invasion capacity of tumor cells decreased significantly(P〈0.05). CONCLUSIONS:PKC may be involved in the process of HN4 migration and invasion by regulating cell adhesion through the effect of P120 ctn and E-cad.
出处
《上海口腔医学》
CAS
CSCD
2017年第2期171-174,共4页
Shanghai Journal of Stomatology
基金
厦门医学院自然科学基金(Z2013-02)