ArticleBMC cancer2024
Epithelial-to-mesenchymal transition and NF-kB pathways are promoted by a mutant form of DDB2, unable to bind PCNA, in UV-damaged human cells.
Article in BMC cancer, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- July in focus in HCB: impact of environmental radiation on cells and tissues.Histochemistry and cell biology · 2026Article
- Epigenetic remodeling during UV exposure: high resolution analysis of histone post-translational modifications in a DNA binding protein 2 mutant model.Histochemistry and cell biology · 2026Article
- Anchorage-independent and faster growth in clonal population from UV-irradiated NER-deficient cells.FEBS open bio · 2026Article
- Characteristics and transcriptional regulators of spontaneous epithelial-mesenchymal transition in genetically unperturbed patient-derived non-spindled breast carcinoma.Breast cancer research : BCR · 2024Article
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Authors and funding
7 authors.
Funding
Abstract
backgroundDNA-Damaged Binding protein 2 (DDB2) is a protein involved in the early step of Nucleotide Excision Repair. Recently, it has been reported that DDB2 is involved in epithelial-to-mesenchymal transition (EMT), key process in tumour invasiveness and metastasis formation. However, its role is not completely known.
methodsBoyden chamber and cell adhesion assays, and ICELLigence analysis were performed to detect HEK293 adhesion and invasion. Western blotting and gelatine zymography techniques were employed to assess the EMT protein levels and MMP enzymatic activity. Immunofluorescence analysis and pull-down assays facilitated the detection of NF-kB sub-cellular localization and interaction.
resultsWe have previously demonstrated that the loss of DDB2-PCNA binding favours genome instability, and increases cell proliferation and motility. Here, we have investigated the phenotypic and molecular EMT-like changes after UV DNA damage, in HEK293 clones stably expressing DDB2
conclusionThese results highlight the role of DDB2-PCNA interaction in counteracting EMT since DDB2
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