Effect Of Genistein Combined With Radiontherapy On Cell Proliferation And Apoptosis In Pulmonary Adenocarcinoma A549Cells

Objective： To examine the effect of Genistein combined withradiontherapy on the proliferation， apoptosis and Ape1/Ref1proteinexpression of human pulmonary adenocarcinoma cell line A549.Methods：A549cells were divided into4groups including a controlgroup (cells with no treatment)，a Genistein group (cells treated withGenistein in the dose of0μmol/L，10μmol/L，30μmol/L，60μmol/L，90μmol/L，respectively，for48h)，an IR group (cells treated with a8Gyirradiation) and a Genistein+IR group(cells pretreated with the same dosesof Genistein for24h and with a8Gy irradiation by a linear accelerator andcontinuously cultured for another24h).The cell proliferation wasexamined by methyl thiazolyltetrazolium (MTT) assay to determined amost suitable Genistein concentration combined with radiontherapy.Cell ofapoptosis of4groups was observed by flow cytometry,and Ape1/Ref1protein was measured by Westernblotting.Results： The inhibition rate of cell proliferation was higher in the treatment of30μmol/L，60μmol/L and90μmol/L Genistein combinedwith irradiation than in the same doses of Genistein treatment alone(P<0.05),and the most suitable concentration of Genistein was30μmol/L.Nosignificant difference was found between the cells treated with lowconcentration (10μmol/L) of Genistein combined with irradiation and withirradiation alone ［(26.67±1.26)%vs (24.70±0.72)%，P=0.102］.The earlyapoptotic rates if the IR group and the Genistein+IR group weresignificantly higher than that of the control group［(30.88±7.63)%、(42.98±1.46)%vs (6.80±0.98)%，P<0.05］，while there was no statisticaldifference between the control group and the Genistein group［(12.96±4.99)%vs (6.80±0.98)%，P=0.143］.As compared with theApe1/Ref1protein expression of the control group，the IR group and theGenistein group，that of Genistein+IR group decreased significantly.Conclusion：Genistein (30μmol/L) can enhance the inhibition effectof radiotherapy on A549cell proliferation through the reduction ofApe1/Ref1protein expression.