The Experimental Study Of1,25Dihydroxyvitamin D₃to The Human Breast Cancer Cells MCF-7（ER+） And MDA-MB-231（ER-）

【Objective】 The purpose of this paper is to study the cell proliferationof the breast cancer cell line of Department MCF-7（ER+） and MDA-MB-231（ER-） cell by different concentrations of1,25dihydroxyvitamin D3treatment, and how about the changes of cells’ apoptosis and cellcycle.In the same time, we researched the influence that used1,25dihydroxyvitamin D3and combine tamoxifen on breast cancer cell lines thatER expression status are difference.【Methods】 Use different concentrations of1,25dihydroxyvitaminD3（10×10-7mol/L,5×10-7mol/L,the10×10-8mol/L）and1,25dihydroxyvitaminD3+TAM to deal with the growth in the logarithmic phase of human breastcancer cells Department of MCF-7and MDA-MB-231.Tetrazolium colorimetricmethod （MTT） and cell proliferation was detected,to calculate theinhibition rate of the two cell lines.Using flow cytometry differentconcentrations of1,25（OH）₂D₃and1,25（OH）₂D₃+TAM joint treatment group,at24h,48h,72h three time points after the MCF-7, MDA-MB-231cell cycleand apoptosis rate conditions.【Results】1.MTT assay showed that the proliferation of MCF-7andMDA-MB-231cells is inhibit after added1,25dihydroxy vitamin D3,andwith the increase in drug concentration and duration of action, theinhibition is stronger. The difference was statistically significant（P<0.05）. However, the inhibition of MDA-MB-231is weak. It is showedthat1,25（OH）₂D₃on MCF-7significantly inhibited, and there was a time a dose-dependent.1,25（OH）₂D₃+TAM combination group deal with MCF-7andMDA-MB-231can produce inhibition, and with the increase in drugconcentration and duration of action, the resulting inhibition isstronger. The inhibition rate compared with the monotherapy groupdifference was statistically significant （P<0.05）. Showed that1,25（OH）₂D₃+the TAM joint treatment group on MCF-7and MDA-MB-231hasa more significant inhibition, and there was a time a dose-dependent.2.Different concentrations of1,25（OH）₂D₃acts on the three timepoints （24h,48h,72h） of MCF-7and MDA-MB-231cell cycle, there isa significant change,especially the increase in the proportion of cellsin G₁phase. Compared with the control group, the difference wasstatistically significant （P<0.05）. But MCF-7cells in G₁phase risenhigher than the proportion of MDA-MB-231cells in G₁phase.1,25（OH）2D3+TAM joint treatment group, Role in the three time points （24h,48h,72h） MCF-7and MDA-MB-231cell cycle mainly for the G₁cell ratio increased.The difference was statistically significant compared with themonotherapy group （P<0.05）.3.Different concentrations of1,25（OH）₂D₃role in the three timepoints （24h,48h,72h） of MCF-7, MDA-MB-231early apoptosis rate increased,ompared with the control group,the difference was statisticallysignificant （P <0.05）.But MCF-7compared to MD-MB-231early apoptosisrate increased more significantly, Comparison of two cell lines in theapoptosis of the same drug concentration, the same point of time, Thedifference was statistically significant （P<0.05）.1,25（OH）₂D₃role of+TAM joint treatment group at three time points（24h,48h,72h）MCF-7andMDA-MB-231showed early apoptosis rate rises.The difference wasstatistically significant compared with the monotherapy group （P<0.05）.【Conclusion】1．1,25（OH）₂D₃on human breast cancer cell line MCF-7and MDA-MB-231were significantly reduced in a dose-time-dependent, cell division arrest in G₁phase, and the emergence of the trend of earlyapoptotic.2．1,25（OH）₂D₃+the TAM joint treatment group on human breast cancercell line MCF-7and MDA-MB-231were significantly reduced, theeffectiveness of its role in a dose-time-dependent, and the cell cycle,apoptosis. Compared with monotherapy, combination therapy group on humanbreast cancer cell line MCF-7, MDA-MB-231inhibition, More likely toinduce human breast cancer cell line MCF-7and MDA-MB-231apoptosis.