Hippo signaling regulates microprocessor and links cell-density-dependent miRNA biogenesis to cancer

Cell. 2014 Feb 27;156(5):893-906. doi: 10.1016/j.cell.2013.12.043.

Abstract

Global downregulation of microRNAs (miRNAs) is commonly observed in human cancers and can have a causative role in tumorigenesis. The mechanisms responsible for this phenomenon remain poorly understood. Here, we show that YAP, the downstream target of the tumor-suppressive Hippo-signaling pathway regulates miRNA biogenesis in a cell-density-dependent manner. At low cell density, nuclear YAP binds and sequesters p72 (DDX17), a regulatory component of the miRNA-processing machinery. At high cell density, Hippo-mediated cytoplasmic retention of YAP facilitates p72 association with Microprocessor and binding to a specific sequence motif in pri-miRNAs. Inactivation of the Hippo pathway or expression of constitutively active YAP causes widespread miRNA suppression in cells and tumors and a corresponding posttranscriptional induction of MYC expression. Thus, the Hippo pathway links contact-inhibition regulation to miRNA biogenesis and may be responsible for the widespread miRNA repression observed in cancer.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, Non-P.H.S.

MeSH terms

  • Cell Count
  • Cell Cycle Proteins
  • Cell Line
  • DEAD-box RNA Helicases / metabolism
  • Hippo Signaling Pathway
  • Humans
  • MicroRNAs / genetics
  • MicroRNAs / metabolism*
  • Neoplasms / genetics*
  • Nuclear Proteins / metabolism
  • Protein Serine-Threonine Kinases / metabolism
  • Proto-Oncogene Proteins c-myc / metabolism
  • Signal Transduction
  • Transcription Factors / metabolism
  • Transcriptome

Substances

  • Cell Cycle Proteins
  • MYC protein, human
  • MicroRNAs
  • Nuclear Proteins
  • Proto-Oncogene Proteins c-myc
  • Transcription Factors
  • YY1AP1 protein, human
  • Protein Serine-Threonine Kinases
  • DDX17 protein, human
  • DEAD-box RNA Helicases

Associated data

  • GEO/GSE49384
  • GEO/GSE52276