Flexibility of intracellular estrogen signaling pathway and mechanism of aromatase inhibitor-resistance

点击翻译按钮获取中文摘要

To elucidate the aromatase inhibitor (AI)-resistant mechanism, we established 6 kinds of resistant cell lines having different resistant mechanisms from ERE-GFP introduced MCF-7 cells which we established previously. These resistant cells were established by long-term estrogen depletion and/or androgen supplemented under monitoring ERE-GFP activity. The characterization of these cell lines revealed novel hormonal therapy-resistant mechanisms such as ligand-independent ER activation by phosphorylation from PI3K-Akt pathway, ER activation by estrogen-like androgen metabolite (3bHSD), or androgen receptor-dependent growth mechanism.