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Oestrogen receptor α AF-1 and AF-2 domains have cell population-specific functions in the mammary epithelium

Author

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  • Stéphanie Cagnet

    (Swiss Institute for Experimental Cancer Research, School of Life Sciences, Ecole Polytechnique Fédérale de Lausanne)

  • Dalya Ataca

    (Swiss Institute for Experimental Cancer Research, School of Life Sciences, Ecole Polytechnique Fédérale de Lausanne)

  • George Sflomos

    (Swiss Institute for Experimental Cancer Research, School of Life Sciences, Ecole Polytechnique Fédérale de Lausanne)

  • Patrick Aouad

    (Swiss Institute for Experimental Cancer Research, School of Life Sciences, Ecole Polytechnique Fédérale de Lausanne)

  • Sonia Schuepbach-Mallepell

    (University of Lausanne)

  • Henry Hugues

    (University Hospital of Lausanne)

  • Andrée Krust

    (Institut de Génétique et de Biologie Moléculaire et Cellulaire (CNRS UMR7104; INSERM U596; ULP, Collège de France) and Institut Clinique de la Souris)

  • Ayyakkannu Ayyanan

    (Swiss Institute for Experimental Cancer Research, School of Life Sciences, Ecole Polytechnique Fédérale de Lausanne)

  • Valentina Scabia

    (Swiss Institute for Experimental Cancer Research, School of Life Sciences, Ecole Polytechnique Fédérale de Lausanne)

  • Cathrin Brisken

    (Swiss Institute for Experimental Cancer Research, School of Life Sciences, Ecole Polytechnique Fédérale de Lausanne)

Abstract

Oestrogen receptor α (ERα) is a transcription factor with ligand-independent and ligand-dependent activation functions (AF)-1 and -2. Oestrogens control postnatal mammary gland development acting on a subset of mammary epithelial cells (MECs), termed sensor cells, which are ERα-positive by immunohistochemistry (IHC) and secrete paracrine factors, which stimulate ERα-negative responder cells. Here we show that deletion of AF-1 or AF-2 blocks pubertal ductal growth and subsequent development because both are required for expression of essential paracrine mediators. Thirty percent of the luminal cells are ERα-negative by IHC but express Esr1 transcripts. This low level ERα expression through AF-2 is essential for cell expansion during puberty and growth-inhibitory during pregnancy. Cell-intrinsic ERα is not required for cell proliferation nor for secretory differentiation but controls transcript levels of cell motility and cell adhesion genes and a stem cell and epithelial mesenchymal transition (EMT) signature identifying ERα as a key regulator of mammary epithelial cell plasticity.

Suggested Citation

  • Stéphanie Cagnet & Dalya Ataca & George Sflomos & Patrick Aouad & Sonia Schuepbach-Mallepell & Henry Hugues & Andrée Krust & Ayyakkannu Ayyanan & Valentina Scabia & Cathrin Brisken, 2018. "Oestrogen receptor α AF-1 and AF-2 domains have cell population-specific functions in the mammary epithelium," Nature Communications, Nature, vol. 9(1), pages 1-15, December.
    • Handle: RePEc:nat:natcom:v:9:y:2018:i:1:d:10.1038_s41467-018-07175-0
    DOI: 10.1038/s41467-018-07175-0
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    Cited by:

    1. Patrick Aouad & Yueyun Zhang & Fabio Martino & Céline Stibolt & Simak Ali & Giovanna Ambrosini & Sendurai A. Mani & Kelly Maggs & Hazel M. Quinn & George Sflomos & Cathrin Brisken, 2022. "Epithelial-mesenchymal plasticity determines estrogen receptor positive breast cancer dormancy and epithelial reconversion drives recurrence," Nature Communications, Nature, vol. 13(1), pages 1-17, December.

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