MicroRNA-mediated post-transcriptional regulation plays key roles in somatic cell self-renewal and tumorigenesis. However, the in vivo functions of specific microRNAs in dominant duct gland somatic cell (MaSC) activity and carcinoma formation stay poorly understood. Here we tend to show that miR-31 is extremely expressed in MaSC-enriched duct gland basal cell population and in duct gland tumors, and is regulated by NF-?B signal. we tend to demonstrate that miR-31 promotes duct gland animal tissue proliferation and MaSC enlargement at the expense of differentiation in vivo. Loss of miR-31 compromises duct gland tumour growth, reduces the quantity of cancer stem cells, also as decreases tumor-initiating ability and metastasis to the respiratory organ, supporting its pro-oncogenic operate. MiR-31 modulates multiple signal pathways, together with Prlr/Stat5, TGF? and Wnt/?-catenin. notably, it activates Wnt/?-catenin signal by directly targeting Wnt antagonists, together with Dkk1. significantly, Dkk1 overexpression part rescues miR31-induced duct gland defects. Together, these findings establish miR-31 because the key regulator of MaSC activity and breast tumorigenesis.