ArticleCytoJournal2025
Novel mechanism of tumor metastasis: DDX11-ATAD5 interaction mediates epithelial-mesenchymal transition to promote gallbladder cancer progression.
Article in CytoJournal, 2025. 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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Abstract
Objective: Molecular mechanisms underlying gallbladder cancer (GBC) progression remain incompletely understood. This study aims to investigate the role and molecular mechanism of DEAD/H-box helicase 11 (DDX11)-ATPase family AAA domain containing 5 (ATAD5) protein interaction in GBC pathogenesis. Material and Methods: Cell proliferation, colony formation, and Transwell assays were performed to evaluate the effects of DDX11-ATAD5 interaction in GBC cells. Sequencing data were analyzed to assess DDX11 and ATAD5 expression in GBC tissues, and immunofluorescence co-localization and co-immunoprecipitation assays were conducted to verify the interaction between DDX11 and ATAD5. Subcutaneous xenograft and metastasis models were established to validate their functions Results: Both DDX11 and ATAD5 were upregulated in GBC tissues and exhibited direct protein-protein interaction ( Conclusion: This study reveals a novel molecular mechanism whereby DDX11-ATAD5 interaction promotes GBC progression through EMT activation, providing potential therapeutic targets for GBC diagnosis and treatment.
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