目的 研究尿石素A對(duì)乳腺癌細(xì)胞MCF-7增殖、凋亡的影響并探討其作用機(jī)制。方法 CCK-8法考察不同濃度尿石素A作用12、24、36、48 h對(duì)MCF-7細(xì)胞增殖能力的影響；細(xì)胞凋亡染色法考察20、40 μmol/L的尿石素A對(duì)MCF-7細(xì)胞凋亡的影響；實(shí)時(shí)熒光定量PCR（RT-qPCR）檢測(cè)c-Myc、Cyclin D1、Bcl-2、Bax mRNA的表達(dá)水平；Western blotting法檢測(cè)c-Myc、Cyclin D1、Bcl-2、Bax蛋白的表達(dá)水平。結(jié)果 尿石素A對(duì)MCF-7細(xì)胞增殖具有抑制作用且呈時(shí)間濃度相關(guān)性；細(xì)胞凋亡染色顯示，20、40 μmol/L尿石素A給藥后均能夠誘導(dǎo)MCF-7細(xì)胞凋亡；RT-qPCR及Western blotting結(jié)果顯示，20、40 μmol/L尿石素A能夠顯著降低MCF-7細(xì)胞中c-Myc、Cyclin D1、Bcl-2 mRNA及蛋白的表達(dá)水平（P<0.05、0.01），升高Bax mRNA及蛋白的表達(dá)水平（P<0.05、0.01）。結(jié)論 尿石素A具有抑制MCF-7細(xì)胞增殖并誘導(dǎo)其凋亡的作用，其作用機(jī)制可能與抑制c-Myc、Cyclin D1、Bcl-2表達(dá)，升高Bax表達(dá)水平有關(guān)。

Objective To study the effect of urolith A on the proliferation and apoptosis of MCF-7 in breast cancer cells and to explore its mechanism. Methods The CCK-8 cell viability assay was used to investigate the effect of different concentrations of urolith A on MCF-7 proliferation of breast cancer cells after 12, 24, 36 and 48 h. Apoptosis staining was used to investigate the effect of urolith A at 20 and 40 μmol/L on the apoptosis of MCF-7 in adenocarcinoma cells. Real-time fluorescence quantitative PCR (RTqPCR) was used to detect the expression levels of c-myc, Cyclin D1, bcl-2 and Bax mRNA. Western blotting was used to detect the expression levels of c-myc, Cyclin D1, bcl-2, Bax and other proteins. Results The different concentrations of urolith A inhibited the proliferation of MCF-7 in breast cancer cells in A time-concentration dependent manner. 20, 40 μmol/L Urolith A can induce the apoptosis of MCF-7 in adenocarcinoma cells. RT-qPCR and Western blotting results showed that urolith A at 20 and 40 μmol/L could reduce the expression level of c-myc, Cyclin D1, Bcl-2 gene protein and mRNA in MCF-7 cells (P<0.05 and 0.01), and increase the expression level of Bax gene protein and mRNA (P<0.05 and 0.01). Conclusion Urolith A can inhibit the proliferation of MCF-7 in breast cancer cells and induce its apoptosis, and its mechanism may be related to the inhibition of the expression of cmyc, Cyclin D1, Bcl-2 and other genes, and the increase of the expression level of Bax gene.

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