Catastrophic nuclear envelope collapse in cancer cell micronuclei
By Emily M. Hatch, A. Fischer, Thomas J. Deerinck, M. Hetzer. Cell, 2013
689 citations recorded by the source corpus.
Summary During mitotic exit missegregated chromosomes can recruit their own nuclear envelope (NE) to form micronuclei (MN). MN have reduced functioning compared to primary nuclei in the same cell, although the two compartments appear to be structurally comparable. Here we show that over 60% of MN undergo an irreversible loss of compartmentalization during interphase due to NE collapse. This disruption of the MN, which is induced by defects in nuclear lamina assembly, drastically reduces nuclear functions and can trigger massive DNA damage. MN disruption is associated with chromatin compaction and invasion of endoplasmic reticulum (ER) tubules into the chromatin. We identified disrupted MN in both major subtypes of human non-small cell lung cancer, suggesting that disrupted MN could be a useful objective biomarker for genomic instability in solid tumors. Our study shows that NE collapse is a key event underlying MN dysfunction and establishes a link between aberrant NE organization and aneuploidy.
Subfields: Molecular Biology, Pulmonary and Respiratory Medicine
View Paper: https://www.semanticscholar.org/paper/954431a487bb3ff6a1d57aedf7c54b31739838cc
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In Molecular Biology
In Pulmonary and Respiratory Medicine
Citations in the corpus
- Chromothripsis and kataegis induced by telomere crisis (2015, neutral): “Importantly, micronuclei show frequent nuclear envelope collapse, which could cause the aforementioned abnormalities (Hatch et al., 2013).”
- The cGAS–cGAMP–STING pathway connects DNA damage to inflammation, senescence, and cancer (2018, background): “Micronuclei are originally formed with a nuclear envelope (NE), but more than half the micronuclei lose compartmentalization after mitosis as their NE ruptures (Hatch et al., 2013).”
- cGAS surveillance of micronuclei links genome instability to innate immunity (2017, neutral): “Micronuclei induced by chromosome missegregation were generated pharmacologically by nocodazole treatment as described previously7,18.”