Nature Communications (Feb 2019)

Overexpression of Claspin and Timeless protects cancer cells from replication stress in a checkpoint-independent manner

  • Julien N. Bianco,
  • Valérie Bergoglio,
  • Yea-Lih Lin,
  • Marie-Jeanne Pillaire,
  • Anne-Lyne Schmitz,
  • Julia Gilhodes,
  • Amelie Lusque,
  • Julien Mazières,
  • Magali Lacroix-Triki,
  • Theodoros I. Roumeliotis,
  • Jyoti Choudhary,
  • Jérôme Moreaux,
  • Jean-Sébastien Hoffmann,
  • Hélène Tourrière,
  • Philippe Pasero

DOI
https://doi.org/10.1038/s41467-019-08886-8
Journal volume & issue
Vol. 10, no. 1
pp. 1 – 14

Abstract

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Oncogene-induced replication stress (RS) promotes cancer development. Here, the authors report that cancer cells adapt to oncogene-induced RS by overexpressing downstream components of ATR-CHK1 pathway, Claspin and Timeless, which have protective role at the replication forks independent of their checkpoint function.