RT Journal Article
SR Electronic
T1 Continuous Endoglin (CD105) Overexpression Disrupts Angiogenesis and Facilitates Tumor Cell Metastasis
JF bioRxiv
FD Cold Spring Harbor Laboratory
SP 691824
DO 10.1101/691824
A1 Claudia Ollauri-Ibáñez
A1 Elena Núñez-Gómez
A1 Cristina Egido-Turrión
A1 Laura Silva-Sousa
A1 Alicia Rodríguez-Barbero
A1 José M. López-Novoa
A1 Miguel Pericacho
YR 2019
UL http://biorxiv.org/content/early/2019/07/03/691824.abstract
AB 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.