Cellular senescence mediated by p16INK4A-coupled miRNA pathways

Nucleic Acids Res. 2014 Feb;42(3):1606-18. doi: 10.1093/nar/gkt1096. Epub 2013 Nov 11.

Abstract

p16 is a key regulator of cellular senescence, yet the drivers of this stable state of proliferative arrest are not well understood. Here, we identify 22 senescence-associated microRNAs (SA-miRNAs) in normal human mammary epithelial cells. We show that SA-miRNAs-26b, 181a, 210 and 424 function in concert to directly repress expression of Polycomb group (PcG) proteins CBX7, embryonic ectoderm development (EED), enhancer of zeste homologue 2 (EZH2) and suppressor of zeste 12 homologue (Suz12), thereby activating p16. We demonstrate the existence of a tight positive feedback loop in which SA-miRNAs activate and re-enforce the expression of other SA-miRNA members. In contrast, PcG members restrain senescence by epigenetically repressing the expression of these SA-miRNAs. Importantly, loss of p16 leads to repression of SA-miRNA expression, intimately coupling this effector of senescence to the SA-miRNA/PcG self-regulatory loop. Taken together, our findings illuminate an important regulatory axis that underpins the transition from proliferation to cellular senescence.

Publication types

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

MeSH terms

  • Cells, Cultured
  • Cellular Senescence / genetics*
  • Cyclin-Dependent Kinase Inhibitor p16 / metabolism*
  • Epigenesis, Genetic*
  • Feedback, Physiological
  • Fibroblasts / cytology
  • Fibroblasts / metabolism
  • Gene Silencing
  • Humans
  • MicroRNAs / metabolism*
  • Polycomb-Group Proteins / genetics
  • Polycomb-Group Proteins / metabolism
  • Young Adult

Substances

  • Cyclin-Dependent Kinase Inhibitor p16
  • MicroRNAs
  • Polycomb-Group Proteins