摘要
目的探讨肿瘤多药抗性（ｍｄｒ１）的基因调控及其特异的凋亡机制。方法在建立的ｍｄｒ１肿瘤裸鼠的瘤组织中，采用ＡＢＣ免疫组化法，检测Ｐ－１７０、ｃ－ｍｙｃ、野生型ｐ５３、ｐ１６、Ｆａｓ和Ｂｃ１－２等蛋白的表达。结果发现ｍｄｒ１肿瘤细胞的ｃ－ｍｙｃ表达增强；经抗ｍｄｒ１－ｒｉｂｏｚｙｍｅ部分逆转ＭＤＲ表型后，ｍｄｒ１肿瘤细胞的ｐ５３表达有所升高。结论ｃ－ｍｙｃ、ｐ５３可能参与了对ｍｄｒ１基因表达的调控，其中ｃ－ｍｙｃ可能起着激活ｍｄｒ１基因转录的作用。实验还发现ｍｄｒ１肿瘤细胞的Ｆａｓ蛋白缺失、Ｂｃ１－２表达升高，提示ｍｄｒ１肿瘤可能拥有自己特异的凋亡调节机制。
Objective To clarify the mechanism of gene regulation and specific apoptosis mechanism in the generation of tumormultidrug resistance phenotype. Methods By ABC immunohistochemical analysis, the expression of several tumor genes (c-myc,p16. wild-type p33. Bcl-2 and Fas) ill nude mice bearing MDR tumor (MCF-7/Adr) were detected. Results c-myc-Ag was highlyexpressed in the MDR tumor cells. and the expression of wild-type p53 was increased a little in the MDR tumor after MDRphenotype was reversed partly by the anti-mdrl-ribozyme. Conclusions c-myc and p53 may play a role in modulating mdrl geneexpression, and c-myc may activate the transcription of mdrl gene. The MDR is correlated with a loss of surface Fas-proteinexpression and high expression of Bcl-2-Ag. These results suggest that the MDR tumor may have a specific regulatory mechanism ofapoptosis.
出处
《第一军医大学学报》
CSCD
1999年第5期408-410,共3页
Journal of First Military Medical University
关键词
乳腺癌
MDRL基因
基因调控
基因凋亡
breast cancer
tumour MDR
mdr1 gene
gene regulatiom
apoptosis
