The miR-424(322)/503 cluster orchestrates remodeling of the epithelium in the involuting mammary gland

Genes Dev. 2014 Apr 1;28(7):765-82. doi: 10.1101/gad.237404.114. Epub 2014 Mar 17.

Abstract

The mammary gland is a very dynamic organ that undergoes continuous remodeling. The critical regulators of this process are not fully understood. Here we identify the microRNA cluster miR-424(322)/503 as an important regulator of epithelial involution after pregnancy. Through the generation of a knockout mouse model, we found that regression of the secretory acini of the mammary gland was compromised in the absence of miR-424(322)/503. Mechanistically, we show that miR-424(322)/503 orchestrates cell life and death decisions by targeting BCL-2 and IGF1R (insulin growth factor-1 receptor). Furthermore, we demonstrate that the expression of this microRNA cluster is regulated by TGF-β, a well-characterized regulator of mammary involution. Overall, our data suggest a model in which activation of the TGF-β pathway after weaning induces the transcription of miR-424(322)/503, which in turn down-regulates the expression of key genes. Here, we unveil a previously unknown, multilayered regulation of epithelial tissue remodeling coordinated by the microRNA cluster miR-424(322)/503.

Keywords: BCL2; IGF1R; TGFβ; mammary gland development; miR-424; miR-503.

MeSH terms

  • Animals
  • Cell Death / genetics
  • Cell Line
  • Epithelium / metabolism*
  • Female
  • Gene Expression Regulation, Developmental*
  • Gene Knockout Techniques
  • Humans
  • Mammary Glands, Animal / cytology
  • Mammary Glands, Animal / metabolism*
  • Mice, Knockout
  • MicroRNAs / genetics*
  • MicroRNAs / metabolism*
  • Promoter Regions, Genetic / genetics
  • Proto-Oncogene Proteins c-bcl-2 / metabolism
  • Receptor, IGF Type 1 / metabolism
  • Signal Transduction
  • Transforming Growth Factor beta1 / metabolism
  • Weaning

Substances

  • MIRN424 microRNA, mouse
  • MicroRNAs
  • Proto-Oncogene Proteins c-bcl-2
  • Transforming Growth Factor beta1
  • Receptor, IGF Type 1