ArticleCellular and molecular life sciences : CMLS2017
XPF knockout via CRISPR/Cas9 reveals that ERCC1 is retained in the cytoplasm without its heterodimer partner XPF.
Article in Cellular and molecular life sciences : CMLS, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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The trial behind it
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Who cites it
11 citing papers in PubMed, 23 citations in OpenAlex.
- FB23-2 and Cisplatin Synergize to Inhibit Head and Neck Squamous Cell Carcinoma by Targeting the XPF/ERCC1 Complex.Cancer science · 2026Article
- RCC1 knockdown sensitizes drug-resistant colorectal cancer to 5-fluorouracil or doxorubicin by impairing DNA repair.Cancer drug resistance (Alhambra, Calif.) · 2025Article
- ERCC4: a potential regulatory factor in inflammatory bowel disease and inflammation-associated colorectal cancer.Frontiers in endocrinology · 2024Review
- Review
- The Drug-Resistance Mechanisms of Five Platinum-Based Antitumor Agents.Frontiers in pharmacology · 2020Review
- The balance between NRF2/GSH antioxidant mediated pathway and DNA repair modulates cisplatin resistance in lung cancer cells.Scientific reports · 2019Article
- Nucleotide excision repair of abasic DNA lesions.Nucleic acids research · 2019Article
- Review
- Function and Interactions of ERCC1-XPF in DNA Damage Response.Molecules (Basel, Switzerland) · 2018Review
- Repair protein persistence at DNA lesions characterizes XPF defect with Cockayne syndrome features.Nucleic acids research · 2018Article
- Splice variants of the endonucleases XPF and XPG contain residual DNA repair capabilities and could be a valuable tool for personalized medicine.Oncotarget · 2018Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The XPF/ERCC1 heterodimeric complex is essentially involved in nucleotide excision repair (NER), interstrand crosslink (ICL), and double-strand break repair. Defects in XPF lead to severe diseases like xeroderma pigmentosum (XP). Up until now, XP-F patient cells have been utilized for functional analyses. Due to the multiple roles of the XPF/ERCC1 complex, these patient cells retain at least one full-length allele and residual repair capabilities. Despite the essential function of the XPF/ERCC1 complex for the human organism, we successfully generated a viable immortalised human XPF knockout cell line with complete loss of XPF using the CRISPR/Cas9 technique in fetal lung fibroblasts (MRC5Vi cells). These cells showed a markedly increased sensitivity to UVC, cisplatin, and psoralen activated by UVA as well as reduced repair capabilities for NER and ICL repair as assessed by reporter gene assays. Using the newly generated knockout cells, we could show that human XPF is markedly involved in homologous recombination repair (HRR) but dispensable for non-homologous end-joining (NHEJ). Notably, ERCC1 was not detectable in the nucleus of the XPF knockout cells indicating the necessity of a functional XPF/ERCC1 heterodimer to allow ERCC1 to enter the nucleus. Overexpression of wild-type XPF could reverse this effect as well as the repair deficiencies.
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