Oncogene-induced replication stress drives genome instability and tumorigenesis

Dan Sarni, Batsheva Kerem*

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review

19 Scopus citations

Abstract

Genomic instability plays a key role in driving cancer development. It is already found in precancerous lesions and allows the acquisition of additional cancerous features. A major source of genomic instability in early stages of tumorigenesis is DNA replication stress. Normally, origin licensing and activation, as well as replication fork progression, are tightly regulated to allow faithful duplication of the genome. Aberrant origin usage and/or perturbed replication fork progression leads to DNA damage and genomic instability. Oncogene activation is an endogenous source of replication stress, disrupting replication regulation and inducing DNA damage. Oncogene-induced replication stress and its role in cancer development have been studied comprehensively, however its molecular basis is still unclear. Here, we review the current understanding of replication regulation, its potential disruption and how oncogenes perturb the replication and induce DNA damage leading to genomic instability in cancer.

Original languageAmerican English
Article number1339
JournalInternational Journal of Molecular Sciences
Volume18
Issue number7
DOIs
StatePublished - Jul 2017

Bibliographical note

Publisher Copyright:
© 2017 by the authors. Licensee MDPI, Basel, Switzerland.

Keywords

  • Cancer
  • DNA replication
  • Genomic instability
  • Oncogene
  • Replication stress

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