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A suppressor role for soluble endoglin in cancer

AutorQuintanilla, Miguel ; Castillo, Gaelle del; Sánchez-Blanco, Esther; Martín-Villar, Ester ; Valbuena-Díez, Ana C. ; Langa, Carmen ; Pérez-Gómez, Eduardo ; Renart, Jaime ; Bernabéu, Carmelo
Palabras claveSoluble endoglin
Fecha de publicación2015
EditorSmart Science and Technology
CitaciónCancer Cell & Microenvironment 2(2): e706 (2015)
ResumenElevated levels of a circulating form of the transforming growth factor-β (TGF-β) coreceptor endoglin correlate with poor clinical outcome in different types of cancer. Soluble endoglin (Sol-Eng) is primarily produced by cleavage of cell-surface endoglin by the transmembrane metalloprotease MMP14 that releases most of its extracellular domain. Sol-Eng has been found to contribute to different cardiovascular pathologies, including preeclampsia, a severe hypertensive syndrome of pregnancy. While the anti-angiogenic and pro-hypertensive functions of Sol-Eng appear well established, its role in cancer has not been fully investigated. Recently, we reported that Sol-Eng strongly inhibits signaling through the hepatocyte growth factor (HGF) tyrosine kinase receptor Met in mouse skin spindle carcinoma cells. Sol-Eng also blocked basal and HGF-mediated stimulation of carcinoma cell proliferation, migration and invasion. Taken together, the above results and the anti-angiogenic function exerted by Sol-Eng suggest a suppressor role for Sol-Eng in cancer. This conclusion is discussed in the paradoxical context of Sol-Eng as a marker of poor prognosis and as a potential contributor to the decreased risk of preeclamptic mothers to develop breast cancer later in life.
DescripciónThis work is licensed under a Creative Commons Attribution 4.0 International License.
Versión del editorhttp://dx.doi.org/10.14800/ccm.706
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