摘要
目的:探讨KDM5B对唾液腺腺样囊性癌侵袭、转移能力的调控作用。方法:通过q PCR验证唾液腺腺样囊性癌与正常组织中KDM5B的表达水平差异,以唾液腺腺样囊性癌肺转移细胞株SACC-83为实验对象,通过脂质体介导,将KDM5B-si R转染至SACC-83细胞,降低KDM5B的表达水平。采用荧光实时定量RT-PCR检测转染前、后SACC-83中KDM5B的表达变化,通过Transwell小室检测细胞侵袭、迁移能力的改变,Western印迹检测KDM5B的下游信号分子Akt的表达变化。应用SPSS 16.0软件包对所得数据进行t检验或单因素方差分析。结果:转染KDM5B-si R后的SACC-83中,KDM5B表达显著下调(P<0.01)。SACC-83细胞的侵袭、迁移能力显著降低(P<0.01)。Western印迹检测结果显示,在SACC-83细胞中降低KDM5B的表达水平后,Akt磷酸化水平升高,而Akt的表达水平不变。结论:高表达KDM5B有助于维持ACC的侵袭、转移特性,降低其表达水平则能有效抑制SACC-83的侵袭、迁移能力。KDM5B可能通过调控其下游信号通路基因Akt的磷酸化水平而发挥作用。
PURPOSE: To investigate the function of KDM5 B in regulation of cell invasion and migration of salivary adenoid cystic carcinoma(SACC). METHODS: The expression levels of KDM5 B were detected by real-time PCR in SACC and normal tissues. The changes of cell invasion and migration were detected by Transwell assays. Western blotting was performed to detect the expression of KDM5 B. The data was analyzed using SPSS 16.0 software package. RESULTS:After transfection with KDM5B-si R,the expression of KDM5 B was significantly down-regulated(P〈0.01). The invasion and migration ability of KDM5 B was substantially inhibited by KDM5B-si R.Western blotting showed that KDM5 B was positively expressed in SACC-83. With down-regulation of KDM5 B, the expression of p-Akt was up-regulated substantially in SACC-83. CONCLUSIONS: Overexpression of KDM5 B played an important role in the process of invasion and migration in SACC-83. Down-regulation of KDM5 B in SACC-83 could substantially suppress its ability of invasion and migration. KDM5 B may exert its role by regulating the expression of p-Akt.
出处
《中国口腔颌面外科杂志》
CAS
2017年第1期16-19,共4页
China Journal of Oral and Maxillofacial Surgery
基金
广东省医学科研基金(B2014136)