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- Eduardo Pérez-Gómez
- Instituto de Investigaciones Biomédicas Alberto Sols, Consejo Superior de Investigaciones Científicas (CSIC)-Universidad Autênoma de Madrid, Madrid, Spain
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- Gaelle del Castillo
- Instituto de Investigaciones Biomédicas Alberto Sols, Consejo Superior de Investigaciones Científicas (CSIC)-Universidad Autênoma de Madrid, Madrid, Spain
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- Juan Francisco Santibáñez
- Institute for Medical Research, University of Belgrado, Belgrado, Serbia
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- Jose Miguel Lêpez-Novoa
- Instituto Reina Sofía de Investigaciên Nefrolêgica, Departamento de Fisiologia y Farmacología, Universidad de Salamanca, Salamanca, Spain
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- Carmelo Bernabéu
- Centro de Investigaciones Biológicas, CSIC, and CIBER de Enfermedades Raras (CIBERER), Madrid, Spain
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- Miguel Quintanilla
- Instituto de Investigaciones Biomédicas Alberto Sols, Consejo Superior de Investigaciones Científicas (CSIC)-Universidad Autênoma de Madrid, Madrid, Spain
説明
<jats:p>Endoglin (CD105) is an auxiliary membrane receptor of transforming growth factor beta (TGF-β) that interacts with type I and type II TGF-β receptors and modulates TGF-β signaling. Endoglin is overexpressed in the tumor-associated vascular endothelium, where it modulates angiogenesis. This feature makes endoglin a promising target for antiangiogenic cancer therapy. In addition, recent studies on human and experimental models of carcinogenesis point to an important tumor cell–autonomous role of endoglin by regulating proliferation, migration, invasion, and metastasis. These studies suggest that endoglin behaves as a suppressor of malignancy in experimental and human epithelial carcinogenesis, although it can also promote metastasis in other types of cancer. In this review, we evaluate the implication of endoglin in tumor development underlying studies developed in our laboratories in recent years.</jats:p>
収録刊行物
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- The Scientific World JOURNAL
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The Scientific World JOURNAL 10 2367-2384, 2010
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