曲古抑菌素A上调肿瘤细胞柯萨奇-腺病毒受体表达而抑制其侵袭力的体外研究  

Inhibitory effect of Trichostatin A on invasive ability of malignant cell line by up-regulation of the express of coxsackie adenovirus receptor in vitro

作　　者：方勇[1] 王蓓蓓[1] 吴鹏[1] 马晓黎[1] 卢运萍[1] 周剑锋[1] 马丁[1] 

机构地区：[1]华中科技大学同济医学院附属同济医院肿瘤生物医学中心,湖北武汉430030

出　　处：《医学研究生学报》2007年第5期451-454,I0001,共5页Journal of Medical Postgraduates

基　　金：国家自然科学基金资助项目(批准号:30371657);国家973重大基础研究项目基金资助(批准号:2002CB513107)

摘　　要：目的:探讨组蛋白去乙酰化酶抑制剂(HDACI)曲古抑菌素A(TSA)抑制肿瘤细胞侵袭力是否通过上调肿瘤细胞表面柯萨奇-腺病毒受体(CAR)的表达而实现的。方法:在TSA作用T24细胞和MCF-7细胞后,分别检测CAR mRNA和蛋白水平的表达;同时采用体外黏附实验和Boyden小室体外侵袭实验,以评价细胞黏附和侵袭力的改变。结果:TSA作用72 h后,肿瘤细胞CAR mRNA和蛋白表达水平明显上调,细胞间同型黏附增强,侵袭力下降。且这一过程可被CAR特异性抗体部分逆转。结论:TSA可以通过上调CAR而使肿瘤细胞同型黏附增加,侵袭力下降。Objective ：To investigate whether the inhibitory effect of Trichostatin A on invasive ability of malignant cell line by up-regulation of the express of Coxsackie Adenovirus Receptor（CAR）. Methods ： CAR mRNA and protein expression levels on T24 and MCF-7 cell lines after treatment of TSA were detected by reverse transcription-polymerase chain reaction （RT-PCR） and Western blot, and then the cell adhesion assay and Boyden chamber invasion assay in vitro were applied to evaluate the changes. Resuits ： After treatment of TSA, mRNA and protein expression levels of CAR on T24 and MCF-7 cells were obviously increased; CAR mediated homotyprc cell adhesion increased, invasive ability decreased. Furthermore, these changes could be partly reversed by CAR specific antibody. Conclusion：Up-regulation of CAR expression by Trichostatin A mediated homotypic cell adhesion increased and malignant cell invasive ability decreased.

关 键 词：曲古抑菌素A 柯萨奇-腺病毒受体 同型黏附 侵袭 

分 类 号：R373[医药卫生—病原生物学]