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Aim To determine whether membrane cytokeratin 8(CK8 )and BCRP expression cooperatively contributed to multidrug resistance(MDR)in MCF-7/MX cells.Methods MCF-7/MX cells were transfected with specific anti CK8-siRNAs and anti BCRP-siRNAs via LipofectAMINE2000.The expression of CK8 and BCRP was determined using Western blot,and membrane staining was observed by laser confocal microscopy.Sensitivity to chemical drugs was examined by Sulforhodamine B method.Results The expression levels of cell surface CK8 and BCRP were obviously reduced by siRNAs,and inhibition of CK8 and BCRP expression could effectively restore the sensitivity to drugs and reverse MDR phenotype of MCF-7/MX cells.Conclusions CK8 together with BCRP may play significant roles in conferring the multifactorial MDR phenotype of MCF-7/MX cells,but may act independently via potentially different mechanisms.Combinational approaches that target multiple drug-resistance-related molecules/pathways in cancer cells may represent more efficacious strategies to overcome MDR.
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Purpose:To detect the action of arsenic trioxide(As 2O 3) on the expression of tumor drug-resistant protein. Methods:APL cell line MR 2 resistant to all-trans retinoic acid(ATRA) was used for in vitro studies. APL cell line NB 4 was used for control. The expressions of P-glycoprotein(Pgp), multidrug resistance protein(MRP)were determined by immunocytochemical assays. Results:The expression of Pgp was significantly higher in MR 2 cell line(30%-40%) than in NB 4 cell line(10%-20%)(P
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Objective To explore the mechanism of reversal of mutidrug resistance of GBC-SD cell lines by grape seed polyphenols(GSP).Methods GBC-SD cell lines were used to determine the effect of GSP.MTT assay was adopted to evaluate the cytotoxity(IC_(50)),RT-PCR were used to determine MDR1mRNA,(P-gp),bcl-2 and cellular adriamycin was measured by flow cytometry.Results In non-toxic(3?g/mL) and low toxic(6?g/mL) comcentration of GSP treated group(P