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ATM couples replication stress and metabolic reprogramming during cellular senescence.

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Ataxia telangiectasia mutated (ATM) regulates cellular response to replication stress by altering metabolism. ATM inactivation bypasses senescence, promoting cancer development by restoring nucleotide levels and reprogramming cellular energy pathways.

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Area of Science:

  • Cellular Biology
  • Cancer Research
  • Metabolism

Background:

  • Replication stress from nucleotide deficiency is crucial in cancer initiation.
  • Replication stress typically triggers cellular senescence, a tumor suppression mechanism.
  • Senescence bypass is linked to cancer development and metabolic reprogramming.

Purpose of the Study:

  • To investigate the role of metabolic reprogramming in cellular response to replication stress.
  • To elucidate the function of ataxia telangiectasia mutated (ATM) in coupling replication stress and metabolism.

Main Methods:

  • Investigated the effect of ATM inactivation on cellular senescence.
  • Analyzed changes in deoxyribonucleotide triphosphate (dNTP) levels.
  • Examined metabolic pathway alterations, including the pentose phosphate pathway (PPP), glucose, and glutamine consumption.
  • Assessed the roles of p53 and c-MYC downstream of ATM.

Main Results:

  • ATM inactivation bypasses senescence induced by replication stress.
  • Deoxyribonucleotide triphosphate (dNTP) levels are restored upon ATM inactivation.
  • Upregulation of the pentose phosphate pathway (PPP) via increased glucose-6-phosphate dehydrogenase (G6PD) activity and enhanced glucose/glutamine consumption were observed.
  • These metabolic shifts were mediated by ATM-dependent suppression of p53 and upregulation of c-MYC.

Conclusions:

  • ATM plays a central role in regulating cellular response to replication stress by shifting cellular metabolism.
  • ATM status couples replication stress and metabolic reprogramming during the senescence process.
  • Understanding this link provides insights into cancer development and potential therapeutic strategies.