Indole-3-carbinol disrupts estrogen receptor-alpha dependent expression of insulin-like growth factor-1 receptor and insulin receptor substrate-1 and proliferation of human breast cancer cells.
作者： Crystal N. Marconett , Ankur K. Singhal , Shyam N. Sundar , Gary L. Firestone
DOI: 10.1016/J.MCE.2012.07.008
关键词:
摘要: We previously established that Indole-3-Carbinol (I3C), a natural hydrolysis product of glucobrassicin in cruciferous vegetables, arrests the proliferation estrogen-dependent human breast cancer cells and induces protein degradation Estrogen Receptor-alpha (ERα). demonstrate MCF-7 I3C ablates expression Insulin-like Growth Factor Receptor-1 (IGF1R) Insulin Receptor Substrate-1 (IRS1), downstream effectors IGF1 signaling pathway. Exogenous ERα reversed mediated loss IGF1R IRS1 gene demonstrating down-regulation is functionally linked to control expression. disrupted binding endogenous ERα, but not Sp1, ERE-Sp1 composite elements within IGF1R/IRS1 promoters. abrogated, combined attenuated, cell cycle arrest. Therefore, inhibits estrogen-sensitive through disruption ERα-mediated transcription components cascade.
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