Cruciferous vegetables contain several compounds that can inhibit breast cancer growth and metastasis in the laboratory. Consumption of cruciferous vegetables has been associated with reduced breast cancer risk. Now a new study has reported a mechanism of action by which indole-3-carbinol (I3C) inhibits proliferation of estrogen receptor positive (ER+) breast cancer cells.

Cruciferous vegetables and condiments

While broccoli, brussels sprouts and cabbage are perhaps the most well-known cruciferous vegetable, there are many others:Unlike some other anti-cancer compounds found in foods, those in cruciferous vegetables are relatively bioavailable and meaningful amounts can be obtained through the diet.
The chemopreventive properties of cruciferous vegetables appear to be the result of synergistic interaction of various chemical components. Consuming I3C, DIM, sulforaphane, or broccoli pills appears to be unnecessary to obtain the benefits of cruciferous vegetables, and may be unwise. Isolated cruciferous vegetable components inhibit proliferation of breast cancer cells in the laboratory, but their efficacy and safety in humans needs to be evaluated in large-scale clinical trials.

Latest research explains mechanism of action of I3C

The study referenced at the beginning of this news article was designed to investigate how I3C inhibits proliferation of ER+ breast cancer cells. In previous studies, the authors showed that I3C arrests the proliferation of ER+ human breast cancer cells and induces protein degradation of estrogen receptor-alpha. There are two types of estrogen receptors: estrogen receptor-alpha (ERα) and estrogen receptor-beta (ERβ). Some compounds that bind to ERα do not bind to estrogen ERβ and vice versa.
In the current study, the authors demonstrate that I3C reduces expression of insulin-like growth factor receptor-1 (IGF1R) and insulin receptor substrate-1 (IRS1) in (ER+/PR+) MCF-7 breast cancer cells. Both IGF1R and IRS1 are downstream effectors of the IGF1 signaling pathway. Exogenous ERα reversed I3C-mediated loss of IGF1R and IRS1 gene expression, thereby demonstrating that down-regulation of ERα is linked to I3C control of IGF1R and IRS1 expression. In fact, I3C disrupted binding of endogenous ERα.
The authors conclude that I3C inhibits proliferation of ER+ breast cancer cells through disruption of ERα-mediated transcription of cell signaling components within the IGF1 cascade.