ArticleSignal transduction and targeted therapy2025
Conversion of Ku80 K568 crotonylation to SUMOylation facilitates DNA non-homologous end joining and cancer radioresistance.
Article in Signal transduction and targeted therapy, 2025. 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.
- Article
- Crotonylation of ACAT1 K181 contributes to radioresistance by impacting lactate metabolism.Communications biology · 2026Article
- AEG-1/MTDH Enhances Hepatocellular Carcinoma Radioresistance by Recruiting PTBP1 Via SND1 To Stabilize ATG5 mRNA and Promote Protective Autophagy.Cell biochemistry and biophysics · 2026Article
- Lead Exposure Triggers DNA Damage in TK6 Cells Via Alteration of DNA Repair Gene Expression and Hypermethylation of Ku80 Promoter Region.Biological trace element research · 2026Article
- Methodological Landscape of DNA Damage Response Detection: From Conventional Assays to Future Innovations.Current issues in molecular biology · 2026Review
- hnRNPA1-SF3B3 interaction drives radioresistance in oral squamous cell carcinoma by modulating MARF1 alternative splicing isoforms.Journal of experimental & clinical cancer research : CR · 2026Article
- Review
- Current Perspectives on Radiosensitizers in Cancer Radiotherapy.International journal of nanomedicine · 2026Review
- Exploration of the Immune Microenvironment of Melanoma and Construction of Prognostic Models Based on the Expression Profile of Lysine Crotonylation-Related Genes.International journal of general medicine · 2026Article
- Glutamine metabolism and its roles in tumor radiotherapy by regulating DNA damage repair.Frontiers in cell and developmental biology · 2026Review
- Protein crotonylation in cancer: mechanisms, functions, and therapeutic potential.Cell biology and toxicology · 2025Review
- Non-Histone Lysine Modifications in Tumor Microenvironment: Mechanisms and Therapeutic Opportunities.International journal of molecular sciences · 2025Review
- Decoding the ubiquitin network: molecular mechanisms and therapeutic vulnerabilities for precision radio-sensitization in cancer.Molecular cancer · 2025Review
- Autophagy-Related Proteins in Triple-Negative Breast Cancer: From Molecular Insights to Therapeutic Applications.International journal of molecular sciences · 2025Review
- Advancing Epigenetic Combination Therapy in Oncology: Multifunctional Nano-Drug Delivery Systems for Synergistic Efficacy and Precision Modulation.International journal of nanomedicine · 2025Review
- IGF1R promotes radiation-induced HSCs activation by regulating DNA-PKcs-mediated DNA damage repair.Frontiers in cell and developmental biology · 2025Article
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Authors and funding
22 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chemo-/radioresistance of malignant tumors hampers cancer control and increases patient mortality. Efficient repair of damaged DNA is critical for the maintenance of genomic integrity and fidelity of genetic information. In reverse, increased DNA repair capability in cancer cells contributes to chemo-/radioresistance of malignant tumors. DNA double-strand break (DSB) is the most serious DNA damage and is also the principal molecular basis of radiotherapy. Upon DNA damage, the Ku80 is recruited and forms a critical DNA-PK complex at the DSB sites with Ku70 and the catalytic subunit (DNA-PKcs) to initiate DNA repair. How DNA-PK is assembled and activated is not fully understood. Based on the identification of radiation-reduced Ku80 K568 crotonylation through quantitative global lysine crotonylome analysis, we reveal that Ku80 K568 is crotonylated by p300-CBP-associated factor (PCAF). Upon DNA damage, the K568cr is decrotonylated by HDAC8 (Histone deacetylase 8). Decrotonylation of K568cr empties this site for the subsequent SUMOylation of Ku80 by CBX4. The conversion of Ku80 from K568 crotonylation to SUMOylation facilitates the assembly of DNA-PK complex and autophosphorylation of DNA-PKcs S2056, consequently activating the DSB repair. Moreover, mutation disrupting the post-translational modification (PTM) of Ku80 K568 site sensitizes cancer cells to radiotherapy in tumor-bearing nude mice models. This study elucidates the conversion model between two different forms of PTMs in the regulation of DNA-PK complex assembly and DSB repair, highlighting this model's potential in controlling chemo-/radioresistance of malignant tumors, as well as expands the atlas of therapeutic targets.
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