{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,12,11]],"date-time":"2025-12-11T09:38:29Z","timestamp":1765445909479,"version":"3.46.0"},"reference-count":30,"publisher":"Scientific Scholar","content-domain":{"domain":["cytojournal.com"],"crossmark-restriction":true},"short-container-title":["Cytojournal"],"abstract":"<jats:sec id=\"st1\">\n                    <jats:title>Objective:<\/jats:title>\n                    <jats:p>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)\u2013ATPase family AAA domain containing 5 (ATAD5) protein interaction in GBC pathogenesis.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec id=\"st2\">\n                    <jats:title>Material and Methods:<\/jats:title>\n                    <jats:p>\n                      Cell proliferation, colony formation, and Transwell assays were performed to evaluate the effects of DDX11\u2013ATAD5 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\n                      <jats:italic>in vivo<\/jats:italic>\n                      , and E-cadherin and vimentin were detected by quantitative real-time polymerase chain reaction.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec id=\"st3\">\n                    <jats:title>Results:<\/jats:title>\n                    <jats:p>\n                      Both DDX11 and ATAD5 were upregulated in GBC tissues and exhibited direct protein\u2013protein interaction (\n                      <jats:italic>P<\/jats:italic>\n                      &lt; 0.05). Functional studies revealed that DDX11 promoted GBC cell proliferation, migration, and invasion while inhibiting apoptosis (\n                      <jats:italic>P<\/jats:italic>\n                      &lt; 0.01). ATAD5 silencing markedly attenuated the oncogenic effects mediated by DDX11.\n                      <jats:italic>In vivo<\/jats:italic>\n                      experiments further confirmed that DDX11 overexpression enhanced subcutaneous tumor growth and metastasis in nude mice (\n                      <jats:italic>P<\/jats:italic>\n                      &lt; 0.001). Mechanistically, the DDX11\u2013ATAD5 complex promoted GBC cell invasion and metastasis by facilitating the epithelial-mesenchymal transition (EMT;\n                      <jats:italic>P<\/jats:italic>\n                      &lt; 0.01).\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec id=\"st4\">\n                    <jats:title>Conclusion:<\/jats:title>\n                    <jats:p>This study reveals a novel molecular mechanism whereby DDX11\u2013ATAD5 interaction promotes GBC progression through EMT activation, providing potential therapeutic targets for GBC diagnosis and treatment.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.25259\/cytojournal_42_2025","type":"journal-article","created":{"date-parts":[[2025,12,11]],"date-time":"2025-12-11T09:33:46Z","timestamp":1765445626000},"page":"102","update-policy":"https:\/\/doi.org\/10.25259\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Novel mechanism of tumor metastasis: DDX11\u2013ATAD5 interaction mediates epithelial\u2013mesenchymal transition to promote gallbladder cancer progression"],"prefix":"10.25259","volume":"22","author":[{"given":"Lei","family":"Kong","sequence":"first","affiliation":[{"name":"Department of General Surgery, Ruijin Hospital, School of Medicine, Shanghai Jiaotong University, Jining City, Shandong, China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Wei","family":"Li","sequence":"additional","affiliation":[{"name":"Department of General Surgery, Shanghai Putuo District Central Hospital, Shanghai, China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Weishu","family":"Kong","sequence":"additional","affiliation":[{"name":"Jining Medical University, Jining City, Shandong, China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Huali","family":"Yang","sequence":"additional","affiliation":[{"name":"Department of Ultrasonography, Ruijin Hospital, School of Medicine, 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