Abstract
Adriamycin resistant cells were obtained from low dosage treated BABL/c mice inoculated with S-180 cells. Resistance of these cells for adriamycin was 66-fold more than their parental cells. The resistance for a typical DNA topoisomerase II inhibitor VP16 (Etoposide) was increased 9 times. Overexpression of multidrug resistant gene (MDR gene) products, P-glycoproteins (P-l 70), was also demonstrated by immunohistochemistry. Furthermore, the ability of the resistant cells to reduce net cellular drug accumulation measured by flow fluorescence cytometry was 89-fold higher than their parental cells. These results support the hypothesis that the resistance of S-180R cells to adriamycin was mainly due to the overexpression of P-glycoproteins. The S- 180R cells will be useful to select drugs or some other therapeutic strategies to overcome multidrug resistancein vivo.
Similar content being viewed by others
References
Carmichael J, et al. Evaluation of a tetrazolium-based semiautomated colorimetric assay: assessment of chemosensitivity. Cancer Research 1987; 47:936.
Wood W. Suppression of endogenous avidin-biotin activity in tissues and its relevance to biotin avidin system. J Histochem Cytochem 1981; 29:1196.
Alberts B, et al. Germ Cells and fertilization. In: Alberts B. ed. Molecular Biology of the Cell, 1th New York: Carland Publishing Inc. 1983;792.
1987; 3(5):385.
Sugimoto Y, et al. Development of multidrug resistance in rodent cell lines. In: Roninso I B. ed. Molecular and Cellular Biology of Multidrug Resistance in Tumor Cells, 1th New York: Plenum Press. 1991:57.
1992; 7(4):253.
Author information
Authors and Affiliations
Rights and permissions
About this article
Cite this article
Zhang, T., Gao, C., Zhang, L. et al. Development of an adriamycin resistant murine tumor S-180 cell lineIn vivo . Chin J Cancer Res 5, 240–244 (1993). https://doi.org/10.1007/BF03023753
Issue Date:
DOI: https://doi.org/10.1007/BF03023753