ArticleNature cell biology2019
The nucleoskeleton protein IFFO1 immobilizes broken DNA and suppresses chromosome translocation during tumorigenesis.
Article in Nature cell biology, 2019. 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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31 citing papers in PubMed, 62 citations in OpenAlex.
- Diversification of plant specific organellar single-stranded DNA binding genes and their roles in mitochondrial genome rearrangements in Arabidopsis and rice.BMC plant biology · 2026Article
- IQGAP3, the overlooked oncogenic twin of IQGAP1: mapping its interactome and functional roles across cellular signaling and cancer.Cell communication and signaling : CCS · 2026Review
- IFFO1 inhibits breast cancer by coordinating mitochondrial fission and fatty acid synthesis via the LaminA/C-PGC1α axis.Oncogenesis · 2026Article
- KIF2A-mediated microtubule-dependent nuclear envelope invagination drives nonhomologous end joining.Nucleic acids research · 2026Article
- A nucleoskeleton network preserves genomic integrity by promoting NHEJ and restraining chromosome translocations.Nucleic acids research · 2025Article
- Intermediate filament IFFO1 negatively regulates the migration of lung cancer cells by inhibiting the IQGAP3-Cdc42 interaction.Cell death & disease · 2025Article
- Nuclear deformability increases PARPi sensitivity in BRCA1-deficient cells by increasing microtubule-dependent DNA break mobility.Nature communications · 2025Article
- Recruitment and rejoining of remote double-strand DNA breaks for enhanced and precise chromosome editing.Genome biology · 2025Article
- Developing a prognostic model of glutamine metabolism-related genes associated with clinical features and immune status in melanoma.Frontiers in oncology · 2025Article
- Adaptive functions of structural variants in human brain development.Science advances · 2024Article
- Strophanthidin Induces Apoptosis of Human Lung Adenocarcinoma Cells by Promoting TRAIL-DR5 Signaling.Molecules (Basel, Switzerland) · 2024Article
- High-Efficiency Enrichment by Saturating Nanoliters of Protein Affinity Media.Analytical chemistry · 2023Article
- New Facets of DNA Double Strand Break Repair: Radiation Dose as Key Determinant of HR versus c-NHEJ Engagement.International journal of molecular sciences · 2023Review
- Accurate prediction of pan-cancer types using machine learning with minimal number of DNA methylation sites.Journal of molecular cell biology · 2023Article
- SLFN5-mediated chromatin dynamics sculpt higher-order DNA repair topology.Molecular cell · 2023Article
- A-type lamins involvement in transport and implications in cancer?Nucleus (Austin, Tex.) · 2022Review
- Critical DNA damaging pathways in tumorigenesis.Seminars in cancer biology · 2022Review
- Ku70 affects the frequency of chromosome translocation in human lymphocytes after radiation and T-cell acute lymphoblastic leukemia.Radiation oncology (London, England) · 2022Article
- Microarray screening reveals two non-conventional SUMO-binding modules linked to DNA repair by non-homologous end-joining.Nucleic acids research · 2022Article
- Rare variants in IFFO1, DTNB, NLRC3 and SLC22A10 associate with Alzheimer's disease CSF profile of neuronal injury and inflammation.Molecular psychiatry · 2022Article
Corrections and comments
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Authors and funding
17 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chromosome translocation is a major cause of the onset and progression of diverse types of cancers. However, the mechanisms underlying this process remain poorly understood. Here, we identified a non-homologous end-joining protein, IFFO1, which structurally forms a heterotetramer with XRCC4. IFFO1 is recruited to the sites of DNA damage by XRCC4 and promotes the repair of DNA double-strand breaks in a parallel pathway with XLF. Interestingly, IFFO1 interacts with lamin A/C, forming an interior nucleoskeleton. Inactivating IFFO1 or its interaction with XRCC4 or lamin A/C leads to increases in both the mobility of broken ends and the frequency of chromosome translocation. Importantly, the destruction of this nucleoskeleton accounts for the elevated frequency of chromosome translocation in many types of cancer cells. Our results reveal that the lamin A/C-IFFO1-constituted nucleoskeleton prevents chromosome translocation by immobilizing broken DNA ends during tumorigenesis.
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