Micronuclei Elimination in MCF-7 Human Breast Adenocarcinoma Cells

Sutyagina, Oksana; Kisurina-Evgenieva, O. P.; Онищенко, Г. Е.

doi:10.1134/s1990519x19030106

Cited by 2 publications

(3 citation statements)

References 29 publications

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“…54 On the other hand, loss of NPCs results deficient nuclear import and export in mNE. As a consequence, the recruitments of DNA repair factors (eg, 53BP1, Rad51, Rad50, Rad17, BRCA1, MRE11, NBS1, XPC and XPA) and DDR players (eg, ATM and p53) into these micronuclei are significantly blocked, 24,42,43,[55][56][57][58] resulting extensive defects in DNA damage sensing and repair.…”

Section: Micronuclei Prefer For Rapid Mutagenesismentioning

confidence: 99%

“…In addition, chromatins in micronuclei can either be highly compacted, normal or decondensed, 42 probably depends on the integrity of mNE. For instance, lamin‐B deficient micronuclei contain highly condensed chromatin 43 . Micronuclei generated from laggards are less condensed than those generated from chromatin bridges 37 .…”

Section: Not All Micronuclei Are Equal: Heterogeneities In the Sourcementioning

confidence: 99%

“…For instance, lamin-B deficient micronuclei contain highly condensed chromatin. 43 Micronuclei generated from laggards are less condensed than those generated from chromatin bridges. 37 Some micronuclei undergo active DNA end processing to generate single-strand DNA (ssDNA).…”

Section: Introductionmentioning

confidence: 99%

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Small but strong: Mutational and functional landscapes of micronuclei in cancer genomes

Guo

Dai

et al. 2020

Intl Journal of Cancer

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Micronuclei, small spatially-separated, nucleus-like structures, are a common feature of human cancer cells. There are considerable heterogeneities in the sources, structures and genetic activities of micronuclei. Accumulating evidence suggests that micronuclei and main nuclei represent separate entities with respect to DNA replication, DNA damage sensing and repairing capacity because micronuclei are not monitored by the same checkpoints nor covered by the same nuclear envelope as the main nuclei. Thus, micronuclei are spatially restricted "mutation factories." Several large-scale DNA sequencing and bioinformatics studies over the last few years have revealed that most micronuclei display a mutational signature of chromothripsis immediately after their generation and the underlying molecular mechanisms have been dissected extensively. Clonal expansion of the micronucleated cells is contextdependent and is associated with chromothripsis and several other mutational signatures including extrachromosomal circular DNA, kataegis and chromoanasynthesis. These results suggest what was once thought to be merely a passive indicator of chromosomal instability is now being recognized as a strong mutator phenotype that may drive intratumoral genetic heterogeneity. Herein, we revisit the actionable determinants that contribute to the bursts of mutagenesis in micronuclei and present the growing number of evidence which suggests that micronuclei have distinct shortand long-term mutational and functional effects to cancer genomes. We also pose challenges for studying the long-term effects of micronucleation in the upcoming years.

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