CytoJournal · 2025
Novel mechanism of tumor metastasis: DDX11-ATAD5 interaction mediates epithelial-mesenchymal transition to promote gallbladder cancer progression.
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Kong Lei, Li Wei, Kong Weishu, Yang Huali
Аннотация
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 in vivo, and E-cadherin and vimentin were detected by quantitative real-time polymerase chain reaction.
RESULTS: Both DDX11 and ATAD5 were upregulated in GBC tissues and exhibited direct protein-protein interaction (P < 0.05). Functional studies revealed that DDX11 promoted GBC cell proliferation, migration, and invasion while inhibiting apoptosis (P < 0.01). ATAD5 silencing markedly attenuated the oncogenic effects mediated by DDX11. In vivo experiments further confirmed that DDX11 overexpression enhanced subcutaneous tumor growth and metastasis in nude mice (P < 0.001). Mechanistically, the DDX11-ATAD5 complex promoted GBC cell invasion and metastasis by facilitating the epithelial-mesenchymal transition (EMT; P < 0.01).
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.
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 in vivo, and E-cadherin and vimentin were detected by quantitative real-time polymerase chain reaction.
RESULTS: Both DDX11 and ATAD5 were upregulated in GBC tissues and exhibited direct protein-protein interaction (P < 0.05). Functional studies revealed that DDX11 promoted GBC cell proliferation, migration, and invasion while inhibiting apoptosis (P < 0.01). ATAD5 silencing markedly attenuated the oncogenic effects mediated by DDX11. In vivo experiments further confirmed that DDX11 overexpression enhanced subcutaneous tumor growth and metastasis in nude mice (P < 0.001). Mechanistically, the DDX11-ATAD5 complex promoted GBC cell invasion and metastasis by facilitating the epithelial-mesenchymal transition (EMT; P < 0.01).
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.