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.
出处
《医学研究生学报》
CAS
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)
关键词
曲古抑菌素A
柯萨奇-腺病毒受体
同型黏附
侵袭
Trichostatin A
Coxsackie adenovirus receptor
Homotypic cell adhesion
Invasion