Reversal effect of BM-cyclin 1 on multidrug resistance in C-A120 cells

In this study, multidrug-resistant human epidermoid C-A120 cells and the sensitive parental KB cells were used as experimental models. BM-cyclin 1, a traditional antimycoplasma drug, was tested to explore the reversal effect of multidrug resistance and its mechanisms in these cell lines. The MTT analysis showed that BM-cyclin 1 could reverse multidrug resistance effectively in C-A120 cells; the sensitivity of C-A120 cells to adriamycin, etoposide and cisplatin was enhanced by 6.0, 8.2 and 1.7 times, respectively. Immunoblotting analysis and reverse transcription-polymerase chain reaction were used to study the BM-cyclin 1-induced changes in topoisomerase IIalpha. The results showed that the expression of topoisomerase IIalpha in treated C-A120 cells increased significantly. Topoisomerase II catalytic activity increased by 30% compared with the untreated cells, as measured by decatenation of kinetopolast DNA. Immunoblotting analysis also indicated the transcription factor levels of specificity: those of protein 1 (Sp1) and nuclear factor-YA increased after treatment with BM-cyclin 1, whereas the mRNA and protein expression of multidrug resistance protein 2 was significantly downregulated. These results demonstrated that BM-cyclin 1 could effectively reverse the multidrug resistance of C-A120 cells by increasing the expression of topoisomerase IIalpha and by suppressing the expression of multidrug resistance protein 2, strongly suggesting that BM-cyclin 1 is a potential multidrug resistance reversal agent.