西亚试剂：Notch Signaling Regulates Mammary Stem Cell Function and Lu

Notch Signaling Regulates Mammary Stem Cell Function and Luminal Cell-Fate Commitment

Toula Bouras,1,3 Bhupinder Pal,1,3 Fran?ois Vaillant,1 Gwyndolen Harburg,1 Marie-Liesse Asselin-Labat,1 Samantha R. Oakes,1 Geoffrey J. Lindeman,1,2 and Jane E. Visvader1,

1 VBCRC Laboratory, The Walter and Eliza Hall Institute of Medical Research, Parkville, Victoria 3050, Australia
2 Department of Medical Oncology, Royal Melbourne Hospital, Parkville, Victoria 3050, Australia

Summary

The recent identification of mouse mammary stem cells (MaSCs) and progenitor subpopulations has enhanced the prospect of investigating the genetic control of their lineage specification and differentiation. Here we have explored the role of the Notch pathway within the mammary epithelial hierarchy. We show that knockdown of the canonical Notch effector Cbf-1 in the MaSC-enriched population results in increased stem cell activity in vivo as well as the formation of aberrant end buds, implying a role for endogenous Notch signaling in restricting MaSC expansion. Conversely, Notch was found to be preferentially activated in the ductal luminal epithelium in vivo and promoted commitment of MaSCs exclusively along the luminal lineage. Notably, constitutive Notch signaling specifically targeted luminal progenitor cells for expansion, leading to hyperplasia and tumorigenesis. These findings reveal key roles for Notch signaling in MaSCs and luminal cell commitment and further suggest that inappropriate Notch activation promotes the self-renewal and transformation of luminal progenitor cells.

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