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G2/M-Phase Checkpoint Adaptation and Micronuclei Formation as Mechanisms That Contribute to Genomic Instability in

Danî Kalsbeek1, Roy M Golsteyn2

  • 1Cancer Cell Laboratory, Department of Biological Sciences, University of Lethbridge, Lethbridge, AB T1K 3M4, Canada. dani.kalsbeek@uleth.ca.

International Journal of Molecular Sciences
|November 9, 2017
PubMed

Insights

Cancer cells adapt to DNA damage by entering mitosis with errors, leading to genomic instability. This review explores how checkpoint adaptation, micronuclei, and chromothripsis drive cancer evolution and treatment resistance.

Area of Science:

  • Oncology
  • Genetics
  • Cell Biology

Background:

  • Genomic instability is a hallmark of cancer.
  • G2/M-phase checkpoint adaptation, where cells enter mitosis with damaged DNA, contributes to genomic alterations.
  • This process is observed in cancer cells treated with genotoxic agents.

Purpose of the Study:

  • To review the mechanisms of G2/M-phase checkpoint adaptation in cancer.
  • To explore the link between checkpoint adaptation, micronuclei formation, and chromothripsis.
  • To highlight the role of these processes in driving genomic instability and treatment resistance.

Main Methods:

  • Literature review of studies on cancer cell response to genotoxic agents.
  • Analysis of mechanisms involving G2/M-phase checkpoint adaptation.
  • Investigation of the role of micronuclei and chromothripsis in genomic instability.

Main Results:

  • Cancer cells can adapt to genotoxic stress by undergoing checkpoint adaptation, surviving, and forming micronuclei.
  • Micronuclei contain damaged DNA, can replicate, and re-enter the main nucleus.
  • Micronuclei are susceptible to chromothripsis, leading to extensive chromosomal rearrangements.

Conclusions:

  • Checkpoint adaptation, micronuclei formation, and chromothripsis are key contributors to genomic instability in surviving cancer cells.
  • Understanding these mechanisms is crucial for improving cancer treatment outcomes.
  • Targeting these pathways may offer new therapeutic strategies against cancer.
Keywords:
checkpoint adaptationcheckpoint kinase 1 (Chk1)chromothripsiscyclin-dependent kinase 1 (Cdk1)human colon adenocarcinoma (HT-29) cellsmicronuclei

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