期刊
CELL REPORTS
卷 26, 期 10, 页码 2558-+出版社
CELL PRESS
DOI: 10.1016/j.celrep.2019.02.036
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资金
- University of Cambridge
- Cancer Research UK
- ERC Consolidator award [646876]
- CRUK funding
- Susan G. Komen Breast Cancer Foundation scholarship
- European Research Council (ERC) [646876] Funding Source: European Research Council (ERC)
Considerable work has linked hormone receptors, such as estrogen receptor-alpha(ER), with the pioneer factor FOXA1. Altered FOXA1 levels contribute to endocrine-resistant breast cancer, where it maintains ER-chromatin interactions, even in contexts in which cells are refractory to ER-targeted drugs. A recent study controversially suggests that FOXA1 binding can be induced by hormonal pathways, including the estrogen-ER complex. We now show that the vast majority (>99%) of FOXA1 binding events are unaffected by steroid activation. A small number (<1%) of FOXA1 binding sites appear to be induced by estrogen, but these are created from chromatin inter actions between ER binding sites and adjacent FOXA1 binding sites and do not represent genuine new FOXA1-pioneering elements. FOXA1 is therefore not regulated by estrogen and remains a bone fide pioneer factor that is entirely upstream of the ER complex.
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