Cross-resistance to camptothecin analogues in a mitoxantrone-resistant human breast carcinoma cell line is not due to DNA topoisomerase I alterations
作者： Julie K. Horton , Erasmus Schneider , Kenneth H. Cowan , Chih-Hsin J. Yang
DOI:
关键词: Topotecan 、 Mitoxantrone 、 Cancer cell 、 Topoisomerase-I Inhibitor 、 Biochemistry 、 DNA 、 Cell culture 、 Biology 、 Camptothecin 、 Topoisomerase 、 Molecular biology
摘要: We have previously described a mitoxantrone-resistant human breast carcinoma cell line, MCF7/MX, in which resistance was associated with defect the energy-dependent accumulation of mitoxantrone absence P-glycoprotein overexpression (M. Nakagawa et al., Cancer Res. 52: 6175-6181, 1992). now report that this line is highly cross-resistant to camptothecin analogues topotecan (180-fold), 9-aminocamptothecin (120-fold), CPT-11 (56-fold), and SN38 (101-fold), but only mildly parent compound (3.2-fold) 10,11-methylenedioxy-camptothecin (2.9-fold). Topotecan decreased MCF7/MX cells compared parental MCF7/WT cells, there corresponding reduction topotecan-mediated stimulation enzyme/DNA complex formation cells. No multidrug resistance-associated protein detected Furthermore, both sensitive contain equal amounts DNA topoisomerase I protein, relaxation activities were lines inhibited same extent by camptothecin. Thus, these results suggest novel mechanism inhibitors cancer
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