论文部分内容阅读
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。
Objective: To explore the role of protein kinase C (PKC), P120-catenin (P120ctn) and E-cadherin (E-cad) in oral squamous cell carcinoma Interrelationship between cancer and its mechanism in tumor cell invasion and metastasis. METHODS: Transfection of HN4 with plasmid pGFP-V-RS-P120ctnshRNA resulted in a significant decrease of P120ctn expression in HN4 cells. Inhibition of PKC expression by staurosporine (STS) and PKC, P120ctn and E- cad m RNA and protein levels. The changes of tumor cell migration and invasion were detected by Transwell cell invasion assay and cell migration assay before and after inhibition of PKC. SPSS18.0 software package for statistical analysis of the data. Results: When PKC was inhibited by STS, the expression of P120ctn in HN4 / SH P120ctn cells was significantly increased, the expression of E-cad was also increased, and the ability of tumor cells to migrate and invade was significantly decreased (all P <0.05). CONCLUSION: PKC may be involved in the regulation of P120ctn and E-cad expression, which is related to the regulation of cell adhesion, which may play a role in the migration and invasion of HN4 cells.