期刊
ANGIOGENESIS
卷 23, 期 2, 页码 231-247出版社
SPRINGER
DOI: 10.1007/s10456-019-09703-y
关键词
Endoglin; CD105; Angiogenesis; Cancer; Metastasis
资金
- Ministerio de Economia y Competitividad of Spain [SAF2010-15881, SAF2013-45784-R]
- Junta de Castilla y Leon [GR100]
- Kidney Research Network REDINREN [RD06/0016/0013, RD12/0021/0032, RD016/0009/0025]
- Instituto de Salud Carlos III [PI16/00460]
- Instituto de Salud Carlos III (FEDER)
- Fundacion Miguel Casado San Jose
- Fundacion Renal Inigo Alvarez de Toledo
Endoglin (CD105) is an auxiliary receptor for members of the TFG-beta superfamily. Whereas it has been demonstrated that the deficiency of endoglin leads to minor and defective angiogenesis, little is known about the effect of its increased expression, characteristic of several types of cancer. Angiogenesis is essential for tumor growth, so high levels of proangiogenic molecules, such as endoglin, are supposed to be related to greater tumor growth leading to a poor cancer prognosis. However, we demonstrate here that endoglin overexpression do not stimulate sprouting or vascularization in several in vitro and in vivo models. Instead, steady endoglin overexpression keep endothelial cells in an active phenotype that results in an impairment of the correct stabilization of the endothelium and the recruitment of mural cells. In a context of continuous enhanced angiogenesis, such as in tumors, endoglin overexpression gives rise to altered vessels with an incomplete mural coverage that permit the extravasation of blood. Moreover, these alterations allow the intravasation of tumor cells, the subsequent development of metastases and, thus, a worse cancer prognosis.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据