Background and purpose: Multidrug resistance of tumor cells is the main factor for the failure of chemotherapy. It is found that the apigenin has the anti-tumor effect

but its role in multidrug resistant cells was rarely reported. This study aimed to investigate the effect of apigenin on multidrug resistant breast cancer cell line MCF-7/ ADR

and to explore the role of apigenin in reversing multidrug

resistance. Methods: The MCF-7/ADR cells were cultured with different concentrations of apigenin

and the same cells were cultured with ADR in the control group. The cell proliferation was detected by MTT

the cell cycle distribution was detected by PI

and the cell apoptosis was detected by Annexin V/PI. The drug sensitivity in vitro was detected by the method of MTT

and the drug retention rate was detected by rhodamine 123 accumulation. The expression of P-gp protein was measured by Western blot

the RT-PCR method was used to detect the transcription of multidrug resistance gene MDR1. Results: The MCF-7/ADR cell proliferation was inhibited by the apigenin

the cell cycle progression was blocked by the apigenin

and the cell apoptosis was induced by the apigenin. There were significant differences between the apigenin group and the ADR group (P0.05). The IC

50

of ADR on MCF-7/ADR cell was (12.37±0.18) μg/mL with the apigenin effect

while the IC

50

of ADR on MCF-7/ADR cell was (39.83±0.29) μg/mL without the apigenin effect (P0.05). The reversal index was 3.22. The retention rate of rhodamine 123 in MCF-7/ADR cells in the apigenin group was higher than that in the ADR group. The MDR1 gene transcription level in MCF-7/ADR cells was higher than that in the MCF-7 cells

and the P-gp expression in MCF-7/ADR cells was higher than that in the MCF-7 cells. However

the level of MDR1 gene transcription and P-gp expression were down-regulated by the apigenin in the MCF-7/ADR cells. Conclusion: The apigenin had anti-MCF-7/ADR effect

and played the role of reversing multidrug resistance in the MCF-7/ADR cells. The mechanism may be related to down-regulation of the MDR1 gene transcription and the P-gp mediated drug efflux function.