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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 investigate the gene regulation of tumor multidrug resistance (mdr1) and its specific apoptosis mechanism. Methods The expression of P-170, c-myc, wild-type p53, p16, Fas and Bc1-2 proteins was detected by ABC immunohistochemistry in the established tumor tissues of mdr1 tumor nude mice. The results showed that mdr1 tumor cell c-myc expression was enhanced; after mDR1-ribozyme partially reversed the MDR phenotype, mdr1 tumor cell p53 expression was increased. Conclusion c-myc and p53 may be involved in the regulation of mdr1 gene expression, and c-myc may play a role in activating transcription of mdr1 gene. The experiment also found that the mdr1 tumor cell Fas protein deletion, Bcl-2 expression increased, suggesting that mdr1 tumor may have its own specific apoptosis regulation mechanism.