ICT Through The AhR And ER Interaction Response Mechanism Of Restrain Breast Cancer In Vitro Inhibition

Objective:Research Icaritin(ICT) on the role of hydrocarbons receptor (AhR) and ICT through activating of AhR and degradation of ERα protein function in vitro, Preliminary discussion ICT whether it has the role of excited arylhydrocarbons receptors and whether through the arylhydrocarbons receptors and estrogen receptor interaction response on breast cancer MCF-7cell proliferation of molecular mechanism inhibitoryMethods:1. Human breast cancer MCF-7cells culture:In vitro culture human breast cancer cells MCF-7.2. ICT factors of the AhR:Lucifease reporter gene assay and RT-PCR method assay ICT influence of AhR target genes CYP1A1,explore ICT whether it excited about of the AhR.3.Research ICT hormone response effects of AhR and ER interaction:Use of Western-blot analysis, and then observe the combination of ICT and E2, influence of the ERα protein and the cell proliferation in MCF-7cells, Discusses whether ICT through activation of AhR and degradation ERα receptor proteins to inhibit breast cancer cell proliferation initial.Results:l.Luciferase assay results showed that the ICT concentration greater than equal to1μM ICT significantly activates AhR expression.2. By RT-PCR assay show that ICT activation the AhR target genes CYP1A1.3. Western-blot tests result showed that the1μM ICT modulates100pM E2can significantly induced ERα protein degradation, and the results can be protease reversal by inhibitors MG.Conclusions:1. ICT excited about the expression of AhR target genes CYP1A1, but also excited about the role of the ERα.2. ICT modulates E2, significant induce ERα protein degradation, and the results can be protease reversal by inhibitors MG. ICT excited AhR and the response of the AhR-ER inhibitory interaction interaction inhibit the E2induced of the MCF-7cell proliferation.