ArticleJournal of cellular physiology2021
Cancer-associated mutations in the condensin II subunit CAPH2 cause genomic instability through telomere dysfunction and anaphase chromosome bridges.
Article in Journal of cellular physiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 28 citations in OpenAlex.
- Condensin complexes: from chromatin organization to disease.Nucleus (Austin, Tex.) · 2026Review
- Continuous multi-omics pathway enrichment analysis resolves hidden functional heterogeneity.Briefings in bioinformatics · 2026Article
- SMC4/SMAD3/NF-κB axis drives cervical cancer progression and radioresistance via DNA damage repair and immune modulation.Journal of translational medicine · 2026Article
- Review
- NCAPD3 exerts tumor-promoting effects in prostatic cancer via dual impact on miR-30a-5p by STAT3-MALAT1 and MYC.Cell death discovery · 2024Article
- NCAPH drives breast cancer progression and identifies a gene signature that predicts luminal a tumour recurrence.Clinical and translational medicine · 2024Article
- The footprint of gut microbiota in gallbladder cancer: a mechanistic review.Frontiers in cellular and infection microbiology · 2024Review
- NCAPH Drives Breast Cancer Progression and Identifies a Gene Signature that Predicts Luminal A Tumor Recurrence.Research square · 2023Article
- Epigenetic instability caused by absence of CIZ1 drives transformation during quiescence cycles.BMC biology · 2023Article
- DNA methylation variations and epigenetic aging in telomere biology disorders.Scientific reports · 2023Article
- Single-cell transcription profiles in Bloom syndrome patients link BLM deficiency with altered condensin complex expression signatures.Human molecular genetics · 2022Article
- Nuclear envelope, chromatin organizers, histones, and DNA: The many achilles heels exploited across cancers.Frontiers in cell and developmental biology · 2022Review
- Multilevel view on chromatin architecture alterations in cancer.Frontiers in genetics · 2022Review
- Regulation of telomere homeostasis and genomic stability in cancer byScience advances · 2021Article
- Cancer-associated mutations in the condensin II subunit CAPH2 cause genomic instability through telomere dysfunction and anaphase chromosome bridges.Journal of cellular physiology · 2021Article
- A Somatic Mutation-Derived LncRNA Signature of Genomic Instability Predicts Prognosis for Patients With Liver Cancer.Frontiers in surgery · 2021Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Genome instability in cancer drives tumor heterogeneity, undermines the success of therapies, and leads to metastasis and recurrence. Condensins are conserved chromatin-binding proteins that promote genomic stability, mainly by ensuring proper condensation of chromatin and mitotic chromosome segregation. Condensin mutations are found in human tumors, but it is not known how or even if such mutations promote cancer progression. In this study, we focus on condensin II subunit CAPH2 and specific CAPH2 mutations reported to be enriched in human cancer patients, and we test how CAPH2 cancer-specific mutations may lead to condensin II complex dysfunction and contribute to genome instability. We find that R551P, R551S, and S556F mutations in CAPH2 cause genomic instability by causing DNA damage, anaphase defects, micronuclei, and chromosomal instability. DNA damage and anaphase defects are caused primarily by ataxia telangiectasia and Rad3-related-dependent telomere dysfunction, as anaphase bridges are enriched for telomeric repeat sequences. We also show that these mutations decrease the binding of CAPH2 to the ATPase subunit SMC4 as well as the rest of the condensin II complex, and decrease the amount of CAPH2 protein bound to chromatin. Thus, in vivo the R551P, R551S, and S556F cancer-specific CAPH2 mutant proteins are likely to impair condensin II complex formation, impede condensin II activity during mitosis and interphase, and promote genetic heterogeneity in cell populations that can lead to clonal outgrowth of cancer cells with highly diverse genotypes.
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