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Cancer Cells Mobilize Mitochondria to Fuel DNA Repair Under Mechanical Confinement

Targeting the actin–ER scaffold that traps mitochondria at the nuclear edge offers a new strategy to inhibit metastatic spread

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Overview

  • Researchers at the Centre for Genomic Regulation in Barcelona compressed HeLa cells to three microns wide and observed mitochondria racing to form nucleus-associated mitochondria (NAMs) in 84% of confined cells within seconds
  • Live-cell ATP sensors showed NAMs elevate nuclear ATP by about 60% within three seconds of mechanical squeezing to power DNA repair processes
  • DNA damage assays revealed that confined cells with NAM-driven ATP surges repaired double-strand breaks within hours and maintained cell division, whereas cells without this boost failed to proliferate
  • Analysis of breast-tumor biopsies from 17 patients found NAMs in 5.4% of nuclei at invasive fronts versus 1.8% in dense tumor cores, indicating a threefold enrichment where metastasis occurs
  • Disrupting the actin–ER scaffold with latrunculin A collapses NAM formation and reduces ATP surges, and researchers are now seeking drugs to selectively block this scaffold and curb tumor invasiveness