ArticleCell death discovery2026
C/EBPγ induces epithelial-mesenchymal transition and facilitates DNA double-strand break repair in lung adenocarcinoma cells.
Article in Cell death discovery, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Authors and funding
13 authors.
Funding
Abstract
Epithelial-mesenchymal transition (EMT) plays a crucial role in cancer progression and is driven by EMT-inducing transcription factors (EMT-TFs). Although core EMT-TFs are well characterized, transcription factors that couple EMT to malignant phenotypes remain incompletely defined. Here, we identified C/EBPγ as a novel inducer of EMT in lung adenocarcinoma cells by examining regions of extensive histone H3 lysine 4 trimethylation occupancy that are often a hallmark of cellular identity. Ectopic expression of C/EBPγ induced mesenchymal-like morphologies and EMT-associated gene-expression profiles, whereas its RNAi knockdown attenuated EMT. Interestingly, domain mapping showed that the leucine zipper domain, but not the DNA-binding domain, was essential for C/EBPγ-mediated EMT, indicating a novel DNA-binding-independent mechanism involving critical partner proteins. Co-immunoprecipitation and mass spectrometry identified C/EBPβ and the non-homologous end joining (NHEJ) factors XRCC5 and XRCC6 as C/EBPγ-interacting proteins. C/EBPγ promotes EMT, at least in part, by antagonizing the EMT-suppressive activity of C/EBPβ. In parallel, C/EBPγ promoted XRCC6 recruitment to etoposide-induced DNA double-strand break (DSB) sites, enhanced NHEJ activity, facilitated DSB repair, and increased survival under genotoxic stress induced by anticancer drug treatment. Collectively, these findings indicate that C/EBPγ may play a role in linking EMT-associated transcriptional changes with enhanced DNA repair capacity, which could have implications for chemoresistance in lung adenocarcinoma.
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Registered trials
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