CD147 and matrix metallo-proteinase (MMP) 2 and MMP9 expression in multidrug resistant breast cancer cells treated with P-glycoprotein substrate drugs.
- Author:
Qing-quan LI
1
;
Wen-juan WANG
;
Guo-ping XU
;
Xi-xi CAO
;
Jing-da XU
;
Qi CHEN
;
Feng TANG
;
Zu-de XU
Author Information
- Publication Type:Journal Article
- MeSH: ATP-Binding Cassette, Sub-Family B, Member 1; pharmacology; Antineoplastic Agents; pharmacology; Basigin; biosynthesis; genetics; Breast Neoplasms; metabolism; Cell Line, Tumor; Drug Resistance, Multiple; Drug Resistance, Neoplasm; Female; Gene Expression Regulation, Neoplastic; Humans; Matrix Metalloproteinase 2; genetics; metabolism; Matrix Metalloproteinase 9; genetics; metabolism; RNA, Messenger; metabolism
- From: Chinese Journal of Pathology 2007;36(4):247-252
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate effects of P-glycoprotein (gp) substrate drugs on the expression of CD147 and MMP2 and 9 in multidrug resistant breast cancer cells.
METHODSMDR human breast cancer cell line, MCF7/AdrR, and its sensitive parental line, MCF7, were treated with various concentrations of P-gp substrate drugs, including paclitoxel and vincristine, and P-gp nonsubstrate drugs, bleomycin, in serum-free media. At the end of the treatment, expressions of CD147 and MMP2 and 9 were determined by real-time PCR and western blot.
RESULTSIncreased expressions of CD147 and MMP2 and 9 were observed in multidrug resistant cancer cells compared with their parental MCF7 cells. After treatment with bleomycin, the expression of CD147 and MMP2 and 9 in both MCF7 and MCF7/AdrR cells remained unchanged (P > 0.05). However, treatment with paclitoxel and vincristine resulted in a remarkable over-expression of CD147 and MMP2 and 9 at both transcription and protein levels in MCF7/AdrR cell line (P < 0.05), while MCF7 cells failed to show similar response.
CONCLUSIONSP-gp substrate drugs can greatly upregulate the expression of CD147 and MMP2 and 9 in multidrug resistant breast cancer cells, therefore enhancing the tumor metastatic capability.
