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  • Title: Difference between the resistance mechanisms of aclacinomycin- and adriamycin-resistant P388 cell lines.
    Author: Dong J, Naito M, Tatsuta T, Seimiya H, Johdo O, Tsuruo T.
    Journal: Oncol Res; 1995; 7(5):245-52. PubMed ID: 8534930.
    Abstract:
    Aclacinomycin (ACR) is an anthracycline anticancer drug that shows marked effects in Adriamycin (ADM)-resistant tumors. ADM, however, is not effective against ACR-resistant tumor cells. When tumor cells acquire resistance to ACR, though the resistance is not easily acquired, they show strong cross-resistance to ADM. To study the mechanism underlying these phenomena, we studied the resistance mechanism of ACR- and ADM-resistant P388 leukemia cells. The P388/ACR cells showed 4.9- and 100-fold resistance to ACR and ADM, respectively, whereas the P388/ADM cells showed respectively 2.0- and 270-fold resistance. Both P388/ACR and P388/ADM cells expressed large amounts of P-glycoprotein, and the amount was 3-fold higher in the P388/ACR than in the P388/ADM cells. As a result, the accumulation of vincristine and ADM were greatly reduced in P388/ACR and P388/ADM cells, as compared with the parental P388 cells. The accumulation of ACR, however, was moderately reduced in both the resistant cell lines. ACR accumulation in P388/ACR and P388/ADM cells was reduced to respectively 37 and 64% of the level in P388 cells. The amount and the activity of topoisomerase II were comparable in P388 and P388/ACR cells, but they were reduced in P388/ADM cells. Consequently, the formation of protein (topoisomerase II)-DNA cross-links induced by a topoisomerase II inhibitor was more prominent in the P388 and P388/ACR nuclei than in the P388/ADM nuclei. Notably, ACR could reduce the protein-DNA cross-links equally in the nuclei of P388, P388/ACR, and P388/ADM cells.(ABSTRACT TRUNCATED AT 250 WORDS)
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