Ge X, Fares F A, Yannai S
Department of Food Engineering and Biotechnology, Technion-Israel Institute of Technology, Haifa, Israel.
Anticancer Res. 1999 Jul-Aug;19(4B):3199-203.
The anticancer activity of indole-3-carbinol and the possible mechanisms involved were explored in human breast cancer cell lines MCF-7 and T47D. Treatment with indole-3-carbinol suppressed the growth of MCF-7 and T47D cells. MCF-7 cells were more sensitive to indole-3-carbinol than T47D cells. The growth suppression caused by indole-3-carbinol was found to be partially involved in its ability to induce apoptosis (programmed cell death) in MCF-7 cells. Western blot analysis demonstrated that wild-type p53 was not induced after treatment of MCF-7 cells with indole-3-carbinol. Northern blot analysis showed that treatment of MCF-7 cells with indole-3-carbinol did not affect the expression of bax gene (one of the death genes). In the tissue culture medium, indole-3-carbinol was found to be partially converted to 3,3'-diindolylmethane. The experiments indicated that indole-3-carbinol suppressed MCF-7 cell growth in part by induction of apoptosis which was independent of p53 and bax expression and that the effect caused by indole-3-carbinol was partially due to its conversion to a more potent compound, 3,3'-diindolylmethane, in vitro.
在人乳腺癌细胞系MCF - 7和T47D中探究了吲哚 - 3 - 甲醇的抗癌活性及其可能涉及的机制。用吲哚 - 3 - 甲醇处理可抑制MCF - 7和T47D细胞的生长。MCF - 7细胞比T47D细胞对吲哚 - 3 - 甲醇更敏感。发现吲哚 - 3 - 甲醇引起的生长抑制部分与其诱导MCF - 7细胞凋亡（程序性细胞死亡）的能力有关。蛋白质免疫印迹分析表明，用吲哚 - 3 - 甲醇处理MCF - 7细胞后未诱导野生型p53。Northern印迹分析显示，用吲哚 - 3 - 甲醇处理MCF - 7细胞不影响bax基因（死亡基因之一）的表达。在组织培养基中，发现吲哚 - 3 - 甲醇部分转化为3,3'-二吲哚甲烷。实验表明，吲哚 - 3 - 甲醇部分通过诱导凋亡抑制MCF - 7细胞生长，这种凋亡与p53和bax表达无关，并且吲哚 - 3 - 甲醇引起的效应部分归因于其在体外转化为一种更有效的化合物3,3'-二吲哚甲烷。
