Curcumin reverses multidrug resistance of human esophageal cancer Eca-109/VCR cells / 肿瘤

ABSTRACT

Objective: To investigate the reversal effect of curcumin (Cur) on multidrug resistance of human esophageal cancer vincristine (VCR)- resistant Eca-109/VCR cells, and to explore its possible mechanism. Methods: The effects of different concentrations of VCR on the proliferation of parental Eca-109 cells and VCR-resistant Eca-109/VCR cells, as well as the reversal effect of Cur combined with VCR on multidrug resistance of Eca-109/VCR cells were detected by CCK-8 method. The apoptosis rates of Eca-109/VCR cells after treatment with Cur (20 μmol/L) combined with VCR (2 μg/mL) for 6, 12 or 24 h were detected by FCM. The expression level of multiple drug resistance 1 (MDR1) mRNA in Eca-109/VCR cells was measured by real-time fluorescent quantitative PCR. The expression levels of P-glycoprotein (P-gp) and multidrug resistance-related protein (MRP) were detected by immunocytochemistry. Results: The proliferation inhibitory rates of Eca-109/VCR cells were (8.08±0.23)% after treatment with 20 μmol/L Cur for 24 h. The half inhibitory concentration (IC50) of VCR was 0.157 and 2.524 μg/mL in Eca-109 cells and Eca-109/VCR cells, respectively. After treatment with Cur (20 μmol/L) combined with various concentrations of VCR, the drugresistant reversal fold was 3.58 in Eca-109/VCR cells. After treatment with Cur (20 μmol/L) combined with VCR (2 μg/mL) for 12 and 24 h, the apoptosis rates of Eca-109/VCR cells were (11.27±0.21)% and (18.77±0.26)%, which were higher than that in VCR (2 μg/mL) group (both P<0.05). After treatment with Cur (20 μmol/L) combined with VCR (2 or 3 μg/mL) for 24 h, the expression level of MDR1 mRNA in Eca-109/VCR cells was significantly reduced (both P<0.05), and the expression levels of P-gp and MRP were significantly decreased as compared with VCR (2 μg/mL) treatment group (all P<0.05). Conclusion: Cur can reverse multidrug resistance of esophageal cancer Eca-109/VCR cells, and its mechanism may be related to the down-regulation of P-gp and MRP expressions.