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MicroRNA-mediated post-transcriptional regulation plays key roles in stem cell self-renewal and tumorigenesis. However, the in vivo functions of specific microRNAs in controlling mammary stem cell (MaSC) activity and breast cancer formation remain poorly understood. Here we show that  miR-31  is highly expressed in MaSC-enriched mammary basal cell population and in mammary tumors, and is regulated by NF-κB signaling. We demonstrate that  miR-31  promotes mammary epithelial proliferation and MaSC expansion at the expense of differentiation in vivo. Loss of  miR-31  compromises mammary tumor growth, reduces the number of cancer stem cells, as well as decreases tumor-initiating ability and metastasis to the lung, supporting its pro-oncogenic function.  MiR-31  modulates multiple signaling pathways, including Prlr/Stat5, TGFβ and Wnt/β-catenin. Particularly, it activates Wnt/β-catenin signaling by directly targeting Wnt antagonists, including  Dkk1 . Importantly,  Dkk1  overexpression partially rescues  miR31 -induced mammary defects. Together, these findings identify  miR-31  as the key regulator of MaSC activity and breast tumorigenesis.

MiR-31 promotes mammary stem cell expansion and breast tumorigenesis by suppressing Wnt signaling antagonists