title: [Effect of combination of taxol and celecoxib on reversing multidrug resistance human breast cancer cells (MCF-7/ Taxol) and explore its underlying mechanism].
abstract: OBJECTIVE
  To investigate the reversal effect of Celecoxib and Taxol on multidrug resistance (MDR) human breast cancer cells (MCF-7/Taxol) and its underlying mechanism.
  
  
  METHODS
  After establishing the resistance cell lines of human breast cancer on Taxol (MCF-7/Taxol), the effects of the drugs on the toxicity of MCF-7/Taxol cells and the reversal effect of Celecoxib on MDR were determined by CCK-8 assay. The cells were divided into seven groups (A: MCF-7; B: MCF-7/Taxol; C: MCF-7/Taxol + 0.03 microg/mL Taxol; D: MCF-7/ Taxol + 0 .03 microg/mL Taxol + 3 microg/mL Celecoxib; E: MCF-7/Taxol + 0.03 microg/mL Taxol-6 /g/mL Celecoxib; F: MCF-7/Taxol + 3 microg/mL Celecoxib; G: MCF-7/Taxol + 6 microg/mL Celecoxib). The mRNA levels of MDR1 and BCRP in these treated cells were also determined by reverse transcription-polymerase chain reaction (RT-PCR), the protein levels of P-gp and BCRP in these treated cells were also determined by Western blot method.
  
  
  RESULTS
  Compared with the Taxol control, the cytotoxicity effects was obviously increased by combination of Taxol and Celecoxib (P < 0.05). Compared with the vehicle control, Taxol up-regulated mRNA and protein levels of P-gp, whereas Celecoxib down-regulated mRNA and protein levels of P-gp and BCRP (P < 0.05).
  
  
  CONCLUSIONS
  Celecoxib has reversal effect on MDR in MCF-7/Taxol cells, it's possible mechanism might be related to reduce the protein expression of COX-2, the inhibition of P-gp, BCRP mRNA and protein overexpression.
authors.affiliation: Department of Thyroid and Berast Surgery, West China Hospital, Sichuan University, Chengdu 610041, China.
authors.forename: Qing
authors.initials: Q
authors.lastname: Liu
authors.forename: Xue-Juan
authors.initials: XJ
authors.lastname: Liu
authors.forename: Yu-Juan
authors.initials: YJ
authors.lastname: Chen
authors.forename: Jing
authors.initials: J
authors.lastname: Wang
mesh_terms: D000972:Antineoplastic Agents, Phytogenic / Q000494:pharmacology; D001943:Breast Neoplasms / Q000473:pathology*; D000068579:Celecoxib; D045744:Cell Line, Tumor / Q000187:drug effects; D052246:Cyclooxygenase 2 Inhibitors / Q000494:pharmacology; D018432:Drug Resistance, Multiple / Q000187:drug effects*; D019008:Drug Resistance, Neoplasm / Q000187:drug effects*; D005260:Female; D006801:Humans; D017239:Paclitaxel / Q000494:pharmacology*; D011720:Pyrazoles / Q000494:pharmacology*; D013449:Sulfonamides / Q000494:pharmacology*
chemical_list: D000972:Antineoplastic Agents, Phytogenic; D052246:Cyclooxygenase 2 Inhibitors; D011720:Pyrazoles; D013449:Sulfonamides; D000068579:Celecoxib; D017239:Paclitaxel