Reversal effect of BM-cyclin 1 on multidrug resistance by down-regulating MRP2 in BALB/C nude mice bearing C-A120 cells.
10.1007/s11596-013-1208-6
- Author:
Lin WANG
1
;
Xiao-yun LI
;
Gao-feng JIANG
;
Ji-zhen LIANG
;
Yan SUN
;
Wei LIU
Author Information
1. Department of Oncology, the Fourth Affiliated Hospital of Medical College, Jinan University, Guangzhou Red Cross Hospital, Guangzhou, 510220, China, 56771027@qq.com.
- Publication Type:Journal Article
- MeSH:
Animals;
Antiprotozoal Agents;
pharmacology;
Cell Line, Tumor;
Diterpenes;
pharmacology;
Down-Regulation;
Doxorubicin;
pharmacology;
Drug Resistance, Multiple;
drug effects;
Humans;
Mice;
Mice, Nude;
Minocycline;
pharmacology;
Multidrug Resistance-Associated Proteins;
genetics;
metabolism;
RNA, Messenger;
genetics;
metabolism;
Xenograft Model Antitumor Assays
- From:
Journal of Huazhong University of Science and Technology (Medical Sciences)
2013;33(6):840-844
- CountryChina
- Language:English
-
Abstract:
Our previous study demonstrated that BM-cyclin 1, a traditional anti-mycoplasma drug, could effectively reverse the multidrug resistance (MDR) of C-A120 cells. The present study aims to explore the reversal effect of BM-cyclin 1 on MDR and its mechanisms in BALB/C nude mice bearing C-A120 cells. Immunoblotting analysis and reverse transcription-polymerase chain reaction (RT-PCR) were used to study the change in multidrug resistance-associated protein 2 (MRP2) induced by BM-cyclin 1. We found that the expression levels of MRP2 protein and mRNA in C-A120 cells treated with BM-cyclin 1 were reduced significantly. Chemical colorimetry revealed no significant change in the level of glutathione (GSH). In the xenograft model, the inhibitory rate of C-A120 cells growth in BM-cyclin 1 plus adriamycin (ADM) group was 52%, which was significantly higher than in control group (P<0.01). The immunoblotting and RT-PCR results conclusively demonstrated that BM-cycin 1 could significantly reduce the expression of MRP2 in transplanted tumor. In conclusion, BM-cyclin 1 could effectively reverse the MDR of C-A120 cells in vivo by suppressing the expression of MRP2.
