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Techniques to Induce and Quantify Cellular Senescence
06:51

Techniques to Induce and Quantify Cellular Senescence

Published on: May 1, 2017

The tumor suppressor ING1 contributes to epigenetic control of cellular senescence

María Abad1, Alberto Moreno, Alicia Palacios

  • 1Instituto de Investigaciones Biomédicas "Alberto Sols" CSIC-UAM, E-28029 Madrid, Spain.

Aging Cell
|November 17, 2010
PubMed

Insights

The ING1 tumor suppressor protein triggers cellular senescence, a key tumor-suppressive mechanism, by interacting with chromatin. This finding reveals ING1

Area of Science:

  • Oncology
  • Cell Biology
  • Epigenetics

Background:

  • Cellular senescence is a critical tumor-suppressive mechanism.
  • The role of the p33ING1 tumor suppressor in senescence is not fully understood.

Purpose of the Study:

  • To investigate the role of p33ING1 in regulating cellular senescence in human fibroblasts.
  • To elucidate the molecular mechanisms by which p33ING1 induces senescence.

Main Methods:

  • Investigated p33ING1 function in human primary fibroblasts.
  • Utilized RNA interference to silence p33ING1.
  • Employed point mutants to assess the role of H3K4me3 recognition.
  • Analyzed gene expression profiles of ING1-induced senescence.

Main Results:

  • p33ING1 induces a senescent phenotype in a p53-dependent manner.
  • Endogenous p33ING1 accumulates on chromatin during oncogene-induced senescence.
  • Silencing p33ING1 impairs oncogene-induced senescence.
  • A tumor-associated mutant of p33ING1 loses its senescence-inducing ability.
  • Recognition of the H3K4me3 chromatin mark is essential for p33ING1-mediated senescence.
  • ING1-induced senescence exhibits a genetic signature overlapping with oncogene-induced senescence, enriched in chemokine and cytokine signaling.

Conclusions:

  • ING1 is a critical epigenetic regulator of cellular senescence in human fibroblasts.
  • ING1 controls gene expression during this tumor-protective response.
  • Dysregulation of ING1's senescence-inducing function may contribute to tumorigenesis.

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