Continuous Endoglin (CD105) Overexpression Disrupts Angiogenesis and Facilitates Tumor Cell Metastasis

Angiogenesis is a complex process essential for tumor growth. For this reason, high levels of pro-angiogenic molecules, such as endoglin (CD105), are supposed to be related to greater tumor growth that lead to a poor cancer prognosis. However, we demonstrate here that defects in angiogenesis that can be attributed to high levels of endoglin, lead to development and worsening of cancer disease. Steady endoglin overexpression disrupts the correct stabilization of the endothelium and the recruitment of mural cells. In consequence, endoglin overexpression gives rise to altered vessels that promote the intravasation of tumor cells, the subsequent development of metastases and, thus, a worse cancer prognosis.