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ATM activation in hypoxia - causes and consequences

Monica M Olcina1, Roger Ja Grand2, Ester M Hammond1

  • 1Cancer Research UK/MRC Oxford Institute for Radiation Oncology; Department of Oncology; University of Oxford; Oxford, UK.

Molecular & Cellular Oncology
|June 17, 2016
PubMed

Insights

The DNA damage response pathway, involving ataxia telangiectasia mutated (ATM) kinase, is crucial for genomic integrity. Hypoxia, a stressor in tumors, activates ATM signaling, potentially contributing to cancer development.

Area of Science:

  • Molecular Biology
  • Cancer Biology
  • Cellular Stress Response

Background:

  • The DNA damage response (DDR) is vital for maintaining genomic stability and preventing cancer.
  • Ataxia telangiectasia mutated (ATM) kinase is a key regulator of the DDR, activated by DNA damage.
  • ATM can also be activated by non-DNA damaging stresses, such as hypoxia, which is prevalent in solid tumors.

Purpose of the Study:

  • To review the mechanisms of ATM activation by hypoxia.
  • To discuss the role of hypoxia-driven ATM signaling in tumorigenesis.

Main Methods:

  • Literature review focusing on ATM signaling pathways.
  • Analysis of studies investigating hypoxia and its effects on cellular stress responses.
  • Integration of findings on ATM activation in both DNA-damaging and non-DNA-damaging contexts.

Main Results:

  • Hypoxia, particularly severe levels in tumors, induces replication stress.
  • This stress activates DDR pathways, including ATM and ATR signaling.
  • ATM activation by hypoxia, independent of DNA damage, is increasingly recognized.

Conclusions:

  • Hypoxia-induced ATM signaling is a significant pathway in solid tumors.
  • ATM activation in hypoxic tumors may contribute to tumorigenesis.
  • Further research into hypoxia-driven ATM signaling could reveal new therapeutic strategies.
Keywords:
ATMChromatin,DNA damage,HypoxiaReplication

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