Mammary stem cells articles from across Nature Portfolio

Aging-related cancer incidence remains not fully understood. Here, the authors depict a progressive process of senescence in murine mammary stem cells at single-cell resolution, which is governed by the transcription factor Bcl11b and associated with enhanced chemical-induced tumorigenesis in aged mice.

Mammary epithelial cells act to continuously renew the mammary tissue and must balance differentiation and self-renewal. Here they show that Mcam, a non-canonical Wnt pathway member, regulates communication between macrophages and mammary epithelial cells, thereby maintaining self-renewal and subsequently promoting mammary ductal morphogenesis.

Rocha and co-authors show that loss of luminal Rank signaling causes abnormal alveolar differentiation and lactation failure. Subsequent pregnancies activate bipotency in basal cells, replacing unfit luminal cells, and restoring lactation.

TGFβ signalling is reported to regulate hormone-responsive mammary epithelial progenitors that are associated with breast cancer risk. Here, the authors find that short-term TGFBR1 inhibition prevents tumour formation in rat breast cancer models and identify a TGFBR1 inhibition-responsive sub-population of mammary epithelial cells, which is associated with human breast cancer risk.

In this Tools of the Trade article, Lei Yuan (from the Cai lab) highlights a new culture system that allows in vitro reconstitution of a dynamic miniature mammary gland.

XIST loss causes partial gene reactivation at the inactive X chromosome, resulting in Mediator-dependent expansion of adult mammary stem cells and tumorigenesis.

Mitochondria are asymmetrically distributed to the daughter cells according to their age. A study now identifies metabolic features associated with mitochondrial age that regulate cell fate decisions.

The establishment of the two distinct lineages that form the branched epithelial ductal tree of the mammary gland is a complex and essential developmental process. Two independent studies now describe the switch from multipotency to unipotency as an embryonic process and outline mechanisms of early lineage restriction.

Little is known regarding how the interactions of stem cells with the immune system regulate their plasticity. A study now describes a mechanism by which normal breast and cancer stem cells utilize miR-199a to downregulate the corepressor LCOR and minimize responses to type I interferon.