期刊
THESCIENTIFICWORLDJOURNAL
卷 10, 期 -, 页码 2367-2384出版社
HINDAWI LTD
DOI: 10.1100/tsw.2010.230
关键词
endoglin (CD105); TGF-beta; angiogenesis; cancer; migration; invasion; malignant progression
资金
- Spanish Ministry of Science and Innovation [SAF2007-63821, SAF2007-63893, SAF2007-61827]
- Instituto de Salud Carlos III [ISCIII-CIBER CB/06/07/0038, ISCIII-RD06/0016]
- Centro de Investigacion Biomedica en Red de Enfermedades Raras (CIBERER)
- Scientific Foundation of the Asociacion Espanola contra el Cancer
Endoglin (CD105) is an auxiliary membrane receptor of transforming growth factor beta (TGF-beta) that interacts with type I and type II TGF-beta receptors and modulates TGF-beta 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.
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