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目的 : 探讨大豆异黄酮抑制 BCa P- 37乳腺癌细胞增殖的分子机制。方法 : 选择二羟异黄酮、三羟异黄酮处理 BCa P- 37细胞 ,采用生长曲线3H- Td R掺入试验及流式细胞分析等实验方法 ,观察大豆异黄酮对乳腺癌细胞 BCa P- 37增殖的抑制作用 ,同时用转化生长因子 (TGP) β拮抗试验、Western blot分析 ,检测 TGFβ1、TGFβ2 及受体的表达变化情况。结果 : (1～ 9)× 1 0 -5mol/L三羟异黄酮作用 3～ 4d可抑制 BCa P- 37细胞增殖 ,细胞受阻于 G1期 ,且 BCa P- 37细胞的TGFβ1、TGFβ2 及受体表达呈时间剂量依赖性增加。而二羟异黄酮处理组不明显。结论 : 三羟异黄酮抑制 BCa P- 37细胞增殖能力强于二羟异黄酮 ,三羟异黄酮可能通过诱导 TGF-β和 TGF-β受体表达的增加而抑制人乳腺癌细胞 BCa P- 37增殖
Objective : To investigate the molecular mechanism of soy isoflavones inhibiting the proliferation of BCa P-37 breast cancer cells. Methods: BGA P-37 cells were treated with genistein and genistein. The growth curve 3H-Td R incorporation assay and flow cytometric analysis were used to observe the effect of soy isoflavones on breast cancer cells BCa P-37. The inhibitory effect of proliferation was examined simultaneously with transforming growth factor (TGP) β antagonistic assay and Western blot analysis to detect the expression changes of TGFβ1, TGFβ2 and its receptors. Results: (1～9)× 1 0 -5mol/L genistein treatment for 3～4d inhibited the proliferation of BCa P-37 cells, the cells were blocked at G1 phase, and TGFβ1, TGFβ2 and receptors of BCa P-37 cells. The expression was dose-dependently increased in time. The glycoside treatment group was not obvious. Conclusion: Genistein inhibits the proliferation of BCa P-37 cells more strongly than genistein, and genistein may inhibit human breast cancer cells BCa P-37 by inducing the increase of TGF-β and TGF-β receptor expression. proliferation