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为探讨肿瘤细胞多药耐药(MDR)形成的分子机理,本文观察了mdr-1、bcl-2和bax基因及其编码蛋白在人红白血病细胞株K562/ADM中的可能共表达。结果显示,在K562/ADM细胞中,在以mdr-1及P-gp过度表达为 特征的MDR形成时,其bcl-2及产物Bcl-2也过度表达,其中Bcl-2的表达阳性率约为相应敏感株K562的11倍;而Bax在二种细胞中均呈阳性表达,但无显著差异(P>0.05),提示bcl-2基因在mRNA和蛋白水平上的过度表达可能是K562/ADM细胞MDR形成时细胞凋亡耐受的分子基础。
In order to investigate the molecular mechanism of multidrug resistance (MDR) formation in tumor cells, the possible co-expression of mdr-1, bcl-2 and bax genes and their encoded proteins in human leukemia cell line K562/ADM was observed. The results showed that in K562/ADM cells, the expression of bcl-2 and product Bcl-2 were over-expressed in MDRs characterized by over-expression of mdr-1 and P-gp, and the positive rate of Bcl-2 expression was approximately. Was 11 times of the corresponding sensitive strain K562; while Bax was positively expressed in both cells, but there was no significant difference (P>0.05), suggesting that overexpression of bcl-2 mRNA and protein levels may be K562/ADM The molecular basis of apoptosis tolerance in cell MDR formation.