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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

Oncogene-induced senescence is part of the tumorigenesis barrier imposed by DNA damage checkpoints

Jirina Bartkova1, Nousin Rezaei, Michalis Liontos

  • 1Institute of Cancer Biology and Centre for Genotoxic Stress Research, Danish Cancer Society, DK-2100 Copenhagen, Denmark. jb@cancer.dk

Nature
|December 1, 2006
PubMed

Insights

Tumorigenesis barriers, including oncogene-induced senescence, are linked to DNA replication stress. This stress, involving DNA damage and double-strand breaks, acts as a barrier against cancer progression.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Tumorigenesis is hindered by barriers that impede preneoplastic lesion progression.
  • Two known barriers are DNA replication stress and oncogene-induced senescence.
  • The interplay between these barriers remains unclear.

Purpose of the Study:

  • To investigate the relationship between oncogene-induced senescence and DNA replication stress.
  • To determine if DNA replication stress contributes to senescence.
  • To assess the role of these barriers in preventing malignant progression.

Main Methods:

  • Analysis of DNA replication fork dynamics and DNA double-strand breaks in senescent cells.
  • Inhibition of the ataxia telangiectasia mutated (ATM) kinase in a mouse model.
  • Examination of DNA damage and senescence markers in human precancerous lesions.

Main Results:

  • Oncogene-induced senescence exhibits markers of DNA replication stress, including stalled replication forks and DNA double-strand breaks.
  • ATM inhibition reduced senescence induction and increased tumor size and invasiveness in mice.
  • Human precancerous lesions showed co-localization of DNA damage and senescence markers.

Conclusions:

  • Senescence in preneoplastic lesions is a consequence of oncogene-induced DNA replication stress.
  • This senescence, alongside apoptosis, functions as a critical barrier to malignant tumor development.

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