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KAIST Links Enlarged Cancer Nuclei to Replication Stress That Slows Metastasis in Mice

Peer-reviewed PNAS experiments trace a transient nuclear growth to intranuclear actin polymerization with accompanying chromatin reorganization.

Overview

  • Researchers report that DNA replication stress triggers actin polymerization inside the nucleus, directly causing nuclear hypertrophy.
  • Cancer cells in this hypertrophic state showed reduced motility and lower metastatic ability in mouse xenograft models.
  • Hi-C analysis revealed shifts in 3D chromatin topology, indicating a structural reconfiguration rather than a simple size increase.
  • The study used gene-function screening, transcriptomics, 3D genome mapping and in vivo assays, and was published online Sept. 9 in PNAS.
  • The team proposes nuclear structural features as potential diagnostic indicators or therapeutic targets, with clinical validation still needed.