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© 2021 The Authors. ; Rank signaling enhances stemness in mouse and human mammary epithelial cells (MECs) and mediates mammary tumor initiation. Mammary tumors initiated by oncogenes or carcinogen exposure display high levels of Rank and Rank pathway inhibitors have emerged as a new strategy for breast cancer prevention and treatment. Here, we show that ectopic Rank expression in the mammary epithelia unexpectedly delays tumor onset and reduces tumor incidence in the oncogene-driven Neu and PyMT models. Mechanistically, we have found that ectopic expression of Rank or exposure to Rankl induces senescence, even in the absence of other oncogenic mutations. Rank leads to DNA damage and senescence through p16/p19. Moreover, RANK-induced senescence is essential for Rank-driven stemness, and although initially translates into delayed tumor growth, eventually promotes tumor progression and metastasis. We uncover a dual role for Rank in the mammary epithelia: Rank induces senescence and stemness, delaying tumor initiation but increasing tumor aggressiveness. ; This work was supported by grants to E. González-Suárez by the Agencia Estatal de Investigación (AEI) (SAF2014-55997-R, SAF2017-86117-R) co-funded by FEDER funds/European Regional Development Fund (ERDF) (a way to build Europe), by the European Research Council (ERC) under the European Union's Horizon 2020 research and innovation programme (grant agreement no. 682935), and by the Fundació La Marató de TV3. We thank CERCA Programme/Generalitat de Catalunya for institutional support. S. Benítez was a recipient of an FPI, A. Collado-Solé holds an FPU from the MICINN and J Redondo-Pedraza is a recipient of an FPI Severo Ochoa Fellowship. We are grateful to Amgen for providing Rankl and Rankt+/tg mice.