ArticleCell cycle (Georgetown, Tex.)2016
Cancer cells that survive checkpoint adaptation contain micronuclei that harbor damaged DNA.
Article in Cell cycle (Georgetown, Tex.), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 58 citations in OpenAlex.
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- Bromodomain protein BRD4 directs mitotic cell division of mouse fibroblasts by inhibiting DNA damage.iScience · 2024Article
- FEN1 Inhibition as a Potential Novel Targeted Therapy against Breast Cancer and the Prognostic Relevance of FEN1.International journal of molecular sciences · 2024Article
- The cGAS/STING signaling pathway: a cross-talk of infection, senescence and tumors.Cell cycle (Georgetown, Tex.) · 2023Article
- The cyclic guanosine monophosphate synthase-stimulator of interferon genes pathway as a potential target for tumor immunotherapy.Frontiers in immunology · 2023Review
- Chromosomal Instability as Enabling Feature and Central Hallmark of Breast Cancer.Breast cancer (Dove Medical Press) · 2023Review
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- Cleavage of Early Mouse Embryo with Damaged DNA.International journal of molecular sciences · 2022Article
- cGAS/STING cross-talks with cell cycle and potentiates cancer immunotherapy.Molecular therapy : the journal of the American Society of Gene Therapy · 2022Review
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- CHK1 protects oncogenic KRAS-expressing cells from DNA damage and is a target for pancreatic cancer treatment.Cell reports · 2021Article
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- Isolation of a natural product with anti-mitotic activity from a toxic Canadian prairie plant.Heliyon · 2021Article
- Autophagy-Mediated Clearance of Free Genomic DNA in the Cytoplasm Protects the Growth and Survival of Cancer Cells.Frontiers in oncology · 2021Article
- Alerting the immune system to DNA damage: micronuclei as mediators.Essays in biochemistry · 2020Review
- Review
- The CINs of Polo-Like Kinase 1 in Cancer.Cancers · 2020Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We have examined the relationship between checkpoint adaptation (mitosis with damaged DNA) and micronuclei. Micronuclei in cancer cells are linked to genomic change, and may induce chromothripsis (chromosome shattering). We measured the cytotoxicity of the cancer drug cisplatin in M059K (glioma fibroblasts, IC50 15 μM). Nearly 100% of M059K cells were positive for histone γH2AX staining after 48 h treatment with a cytotoxic concentration of cisplatin. The proportion of micronucleated cells, as confirmed by microscopy using DAPI and lamin A/C staining, increased from 24% to 48%, and the total micronuclei in surviving cells accumulated over time. Promoting entry into mitosis with a checkpoint inhibitor increased the number of micronuclei in cells whereas blocking checkpoint adaptation with a Cdk inhibitor reduced the number of micronuclei. Interestingly, some micronuclei underwent asynchronous DNA replication, relative to the main nuclei, as measured by deoxy-bromo-uracil (BrdU) staining. These micronuclei stained positive for histone γH2AX, which was linked to DNA replication, suggesting that micronuclei arise from checkpoint adaptation and that micronuclei may continue to damage DNA. By contrast the normal cell line WI-38 did not undergo checkpoint adaptation when treated with cisplatin and did not show changes in micronuclei number. These data reveal that the production of micronuclei by checkpoint adaptation is part of a process that contributes to genomic change.
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