{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,1,23]],"date-time":"2026-01-23T05:56:13Z","timestamp":1769147773956,"version":"3.49.0"},"reference-count":48,"publisher":"Proceedings of the National Academy of Sciences","issue":"6","content-domain":{"domain":["www.pnas.org"],"crossmark-restriction":true},"short-container-title":["Proc. Natl. Acad. Sci. U.S.A."],"published-print":{"date-parts":[[2010,2,9]]},"abstract":"<jats:p>\n            A single nucleotide polymorphism in the\n            <jats:italic>DAB2IP<\/jats:italic>\n            gene is associated with risk of aggressive prostate cancer (PCa), and loss of DAB2IP expression is frequently detected in metastatic PCa. However, the functional role of DAB2IP in PCa remains unknown. Here, we show that the loss of DAB2IP expression initiates epithelial-to-mesenchymal transition (EMT), which is visualized by repression of E-cadherin and up-regulation of vimentin in both human normal prostate epithelial and prostate carcinoma cells as well as in clinical prostate-cancer specimens. Conversely, restoring DAB2IP in metastatic PCa cells reversed EMT. In DAB2IP knockout mice, prostate epithelial cells exhibited elevated mesenchymal markers, which is characteristic of EMT. Using a human prostate xenograft-mouse model, we observed that knocking down endogenous DAB2IP in human carcinoma cells led to the development of multiple lymph node and distant organ metastases. Moreover, we showed that DAB2IP functions as a scaffold protein in regulating EMT by modulating nuclear \u03b2-catenin\/T-cell factor activity. These results show the mechanism of DAB2IP in EMT and suggest that assessment of DAB2IP may provide a prognostic biomarker and potential therapeutic target for PCa metastasis.\n          <\/jats:p>","DOI":"10.1073\/pnas.0908133107","type":"journal-article","created":{"date-parts":[[2010,1,14]],"date-time":"2010-01-14T03:16:28Z","timestamp":1263438988000},"page":"2485-2490","update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":202,"title":["Role of DAB2IP in modulating epithelial-to-mesenchymal transition and prostate cancer metastasis"],"prefix":"10.1073","volume":"107","author":[{"given":"Daxing","family":"Xie","sequence":"first","affiliation":[{"name":"Departments of Urology,"},{"name":"Department of General Surgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430030, China;"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Crystal","family":"Gore","sequence":"additional","affiliation":[{"name":"Departments of Urology,"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jun","family":"Liu","sequence":"additional","affiliation":[{"name":"Radiology,"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Rey-Chen","family":"Pong","sequence":"additional","affiliation":[{"name":"Departments of Urology,"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ralph","family":"Mason","sequence":"additional","affiliation":[{"name":"Radiology,"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Guiyang","family":"Hao","sequence":"additional","affiliation":[{"name":"Radiology,"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Michael","family":"Long","sequence":"additional","affiliation":[{"name":"Radiology,"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Wareef","family":"Kabbani","sequence":"additional","affiliation":[{"name":"Pathology, and"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Luyang","family":"Yu","sequence":"additional","affiliation":[{"name":"Interdepartmental Program in Vascular Biology and Transplantation and Department of Pathology, Yale University School of Medicine, New Haven, CT 06510;"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Haifeng","family":"Zhang","sequence":"additional","affiliation":[{"name":"Interdepartmental Program in Vascular Biology and Transplantation and Department of Pathology, Yale University School of Medicine, New Haven, CT 06510;"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Hong","family":"Chen","sequence":"additional","affiliation":[{"name":"Cardiovascular Biology Research Program, Oklahoma Medical Research Foundation, Oklahoma City, OK, 73104; and"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Xiankai","family":"Sun","sequence":"additional","affiliation":[{"name":"Radiology,"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"David A.","family":"Boothman","sequence":"additional","affiliation":[{"name":"Oncology, University of Texas Southwestern Medical Center, Dallas, TX 75390;"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Wang","family":"Min","sequence":"additional","affiliation":[{"name":"Interdepartmental Program in Vascular Biology and Transplantation and Department of Pathology, Yale University School of Medicine, New Haven, CT 06510;"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jer-Tsong","family":"Hsieh","sequence":"additional","affiliation":[{"name":"Departments of Urology,"},{"name":"Graduate Institute of Cancer Biology, China Medical University, Taichung 404, Taiwan, China"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"341","published-online":{"date-parts":[[2010,1,13]]},"reference":[{"key":"e_1_3_3_1_2","doi-asserted-by":"publisher","DOI":"10.3322\/CA.2007.0010"},{"key":"e_1_3_3_2_2","doi-asserted-by":"publisher","DOI":"10.1038\/nrc822"},{"key":"e_1_3_3_3_2","doi-asserted-by":"publisher","DOI":"10.1038\/nrm1835"},{"key":"e_1_3_3_4_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.devcel.2008.05.009"},{"key":"e_1_3_3_5_2","first-page":"3650","article-title":"Cadherin switching in human prostate cancer progression","volume":"60","author":"Tomita K","year":"2000","unstructured":"K Tomita, et al., Cadherin switching in human prostate cancer progression. 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