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Mitochondrial Relocation Powers DNA Repair in Confined Cancer Cells, Revealing Therapeutic Target

A cytoskeletal–ER scaffold traps mitochondria at the nuclear envelope, triggering an ATP surge that promotes DNA repair; this mechanism offers a new target to limit tumor spread.

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Overview

  • Mechanical squeezing of cancer cells induces formation of nucleus-associated mitochondria (NAMs) at the nuclear periphery within seconds.
  • NAMs trigger a roughly 60% surge in nuclear ATP, enabling efficient DNA repair; cell cycle progression continues despite mechanical stress.
  • Patient breast tumor samples show a threefold higher prevalence of NAMs at invasive fronts compared with dense tumor cores.
  • An actin–endoplasmic reticulum scaffold physically anchors mitochondria to the nucleus; disrupting actin filaments collapses NAM formation, halting the ATP surge.
  • Researchers are now pursuing therapeutic agents that dismantle the scaffold to block the NAM-driven energy boost; this strategy aims to hinder cancer cell invasiveness.