Moscow J A, Townsend A J, Goldsmith M E, Whang-Peng J, Vickers P J, Poisson R, Legault-Poisson S, Myers C E, Cowan K H
Medicine Branch, National Cancer Institute, Bethesda, MD 20892.
Proc Natl Acad Sci U S A. 1988 Sep;85(17):6518-22. doi: 10.1073/pnas.85.17.6518.
The development of multidrug resistance in MCF7 human breast cancer cells is associated with overexpression of P-glycoprotein, changes in activities of several detoxication enzymes, and loss of hormone sensitivity and estrogen receptors (ERs). We have cloned the cDNA for one of the drug-detoxifying enzymes overexpressed in multidrug-resistant MCF7 cells (AdrR MCF7), the anionic isozyme of glutathione S-transferase (GST pi). Hybridization with this GST pi cDNA, GST pi-1, demonstrated that increased GST pi activity in AdrR MCF7 cells is associated with overexpression but not with amplification of the gene. We mapped the GST pi gene to human chromosome 11q13 by in situ hybridization. Since multidrug resistance and GST pi overexpression are associated with the loss of ERs in AdrR MCF7 cells, we examined several other breast cancer cell lines that were not selected for drug resistance. In each of these cell lines we found an inverse association between GST pi expression and ER content. We also examined RNA from 21 primary breast cancers and found a similar association between GST pi expression and ER content in vivo. GST pi mRNA content in 11 ER-positive tumors (less than or equal to 10 fmol/mg of protein) was significantly different from the GST pi content of 10 ER-negative tumors (P = 0.002; Mann-Whitney Wilcoxon test for two independent samples). The finding of similar patterns of expression of a drug-detoxifying enzyme and of ERs in vitro as well as in vivo suggests that ER-negative breast cancer cells may have greater protection against antineoplastic agents conferred by GST pi than ER-positive tumors.
MCF7人乳腺癌细胞多药耐药性的发展与P-糖蛋白的过表达、几种解毒酶活性的变化以及激素敏感性和雌激素受体(ERs)的丧失有关。我们已经克隆了在多药耐药性MCF7细胞(AdrR MCF7)中过表达的一种药物解毒酶的cDNA,即谷胱甘肽S-转移酶(GST pi)的阴离子同工酶。用这种GST pi cDNA(GST pi-1)进行杂交表明,AdrR MCF7细胞中GST pi活性的增加与该基因的过表达有关,而与基因扩增无关。我们通过原位杂交将GST pi基因定位到人类染色体11q13上。由于多药耐药性和GST pi过表达与AdrR MCF7细胞中ERs的丧失有关,我们检测了其他几种未经过耐药性筛选的乳腺癌细胞系。在这些细胞系中的每一个中,我们都发现GST pi表达与ER含量之间呈负相关。我们还检测了21例原发性乳腺癌的RNA,发现在体内GST pi表达与ER含量之间也有类似的相关性。11例ER阳性肿瘤(≤10 fmol/mg蛋白质)中的GST pi mRNA含量与10例ER阴性肿瘤中的GST pi含量有显著差异(P = 0.002;两独立样本的Mann-Whitney Wilcoxon检验)。在体外和体内发现一种药物解毒酶和ERs具有相似的表达模式,这表明ER阴性乳腺癌细胞可能比ER阳性肿瘤对GST pi赋予的抗肿瘤药物具有更强的保护作用。