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To observe the effects of functional inhibition of p-glycoprotein on radiosensitivity of drug-resistant MCF-7/Adr tumor cells.Flow cytometry was used to examine the dynamic changes of apoptosis rate and mitochondrial membrane potential (deltapsim) in verapamil-treated and untreated MCF-7/Adr cells after the X-ray exposure.The apoptotic rate of verapamil-treated cells was 25.53%+/-2.85%, 30.43%+/-2.21%, 39.03%+/-2.60% at 6, 12, and 24 h after X-ray exposure, respectively, and was 16.13%+/-1.16%, 21.73%+/-1.31%, and 27.53%+/-2.55% for the untreated cells. The mean fluorescence intensity of verapamil-treated cells was 75.27+/-4.90, 96.47+/-5.59, 57.77+/-2.55, respectively, at the corresponding time points, in comparison with the intensity of 54.17+/-4.05, 62.30+/-5.93, and 39.53+/-2.65 for the untreated cells. The apoptosis rate and deltapsim of the treated cells were significantly higher than those in the untreated cells at each of the specified time point (P0.01), and in the former cells, the apoptosis rate reached the maximum at 24 h (F=47.870, P=0.000) and the deltapsim at 12 h after X-ray exposure (F=74.485, P=0.000).The radiosensitivity of MCF-7/Adr cells is increased after functional inhibition of p-glycoprotein, possibly in relation to the alteration of deltapsim.

To investigate the expression of c-myc in drug-resistant MCF-7/Adr human breast cancer cells and the counteractive effect of c-myc antisense oligonucleotide on their drug-resistance.Flow cytometry was performed to examine c-myc expression in multi-drug resistant MCF-7/Adr cell line and its parental cell line MCF-7. The IC50 value of doxorubicin was evaluated by MTT assay.MCF-7/Adr cell line was shown to have a significantly higher expression rate of c-myc than its parent cell line MCF-7 (70.48% vs 46.02%). The IC50 value of doxorubicin was (22.00+/-1.92) micomol/L in MCF-7/Adr cells, which was significantly decreased to (9.60+/-1.04) micromol/L (P0.05) after coincubation with 4 micromol/L c-myc antisense oligonecleotide.c-myc expression is up-regulated in MCF-7/Adr cells as compared with their parent cell line MCF-7. Inhibition of c-myc expression may partially reverse the resistance of MCF-7/Adr against doxorubicin, suggesting that c-myc may be involved in the mechanism of drug-resistance of tumor cells.