Endoglin overexpression modulates cellular morphology, migration, and adhesion of mouse fibroblasts

Guerrero-Esteo, Mercedes; Lastres, Pedro; Letamendı́a, Ainhoa; Pérez-Álvarez, María José; Langa, Carmen; López, Leonardo; Fabra, Àngels; García-Pardo, Ángeles; Vera, Sonia; Letarte, Michelle; Bernabéu, Carmelo

doi:10.1016/s0171-9335(99)80046-6

Cited by 89 publications

(64 citation statements)

References 63 publications

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“…Also, protein expression was not examined in Dunning cells, and prior studies have shown the importance of evaluating endoglin protein expression (Pece- Barbara et al, 1999). Consistent with our findings, other investigators show that loss of endoglin protein expression is associated with increased cell migration (Guerrero-Esteo et al, 1999;McAllister et al, 1995). As changes in adhesion and motility are prerequisites for development of prostate cancer metastasis, it will be important to evaluate endoglin's role in vivo in this regard.…”

Section: Discussionsupporting

confidence: 80%

“…Taken together, findings suggest that significant changes in transcriptional processing may be taking place, and warrant further investigation in future studies. Prior studies have implicated endoglin in the regulation of attachment and motility in fibroblast and endothelial cells (Gougos and Letarte, 1990;Guerrero-Esteo et al, 1999;Mcallister et al, 1995). We had recently shown that endoglin was uniquely differentially expressed during prostate cell detachment, amongst 4000 other genes examined (Jovanovic et al, 2001).…”

Section: Discussionmentioning

confidence: 83%

“…It is a 180 kDa homodimeric type I transmembrane protein, which, when over expressed in mouse fibroblasts, leads to decreased cell migration (Guerrero-Esteo et al, 1999). Endoglin is the gene mutated in Hereditary Hemorrhagic Telangiectasia type 1 (HHT1); a disorder characterized by aberrant arteriole -venous (A -V) malformations, presumably due to aberrant endothelial cell motility (McAllister et al, 1995).…”

Section: Introductionmentioning

confidence: 99%

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Over expression of endoglin in human prostate cancer suppresses cell detachment, migration and invasion

et al. 2002

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The regulation of cell adhesion and motility in human prostate is not well understood. We have previously shown that the endoglin gene is differently expressed during changes in prostate cell adhesion. Endoglin is a transmembrane transforming growth factor b binding protein typically expressed by endothelial cells. In this report we demonstrate that endoglin over expression increases prostate cell attachment, while decreasing migration and invasion. Engineered decreases in endoglin expression have opposite effects. While endoglin exerted only relatively small effects upon cell adhesion, large effects upon cell migration and invasion were observed. Endoglin was shown to localize to focal adhesion plaques, consistent with its role in regulating cell adhesion and motility. Loss of endoglin expression in cancer, as compared to normal prostate, was seen in human prostate cell lines. Suppression of endoglin expression in a panel of normal human prostate cell lines led to cell detachment. Endoglin is identified as a regulator of cell adhesion, motility and invasion in human prostate. Loss of endoglin expression appears to be associated with prostate cancer progression, at least in vitro.

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Section: Discussionsupporting

confidence: 80%

Section: Discussionmentioning

confidence: 83%

Section: Introductionmentioning

confidence: 99%

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Over expression of endoglin in human prostate cancer suppresses cell detachment, migration and invasion

et al. 2002

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“…Endoglin is a TGF-β coreceptor that modulates TGF-β-dependent cellular responses (14,15). Most studies on Endoglin have focused on its pro-angiogenic role in endothelial cells, its involvement in vascular remodelling and its role as a marker of the tumour vasculature, but it also plays a direct role in tumourigenesis (16).…”

Section: Introductionmentioning

confidence: 99%

PRH/HHex inhibits the migration of breast and prostate epithelial cells through direct transcriptional regulation of Endoglin

et al. 2013

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“…19,20 Endoglin is an accessory protein in the TGF-␤ receptor complex; it binds TGF-␤ 1 and 3 with high affinity and modulates cellular responses to TGF-␤ in different types of cells. [21][22][23][24][25][26] Moreover, endoglin is the mutated gene for hereditary hemorrhagic telangiectasia type 1, 27 an autosomal dominant disorder characterized by multisystemic vascular dysplasia and recurrent hemorrhage.…”

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confidence: 99%

Lack of specificity of endoglin expression for tumor blood vessels

et al. 2001

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A monoclonal antibody (MAb; A11) has been raised following mouse immunization with cultured human microvascular endothelial cells. The MAb showed a strong positivity within tumor vessels in glioblastoma and breast carcinoma samples, and the distribution was consistent with antigen association with vascular endothelial cells. A purification procedure of the antigen was developed starting from DG-RSV-LT-2, an immortalized human endothelial cell line. Molecular mass, N-terminal sequence of the purified antigen and localization on endothelial cell surface allowed identification with human endoglin (CD105). Flow cytometry analysis of a group of normal and transformed cell lines showed that, besides endothelial cells and myelocytic leukemia cells already shown to be positive, fetal fibroblasts, choriocarcinoma, fibrosarcoma and rhabdomyosarcoma cell lines were also positive for this antigen. Immunohistochemic analysis of several normal adult tissues revealed a more extensive presence of the antigen in normal vessels compared to that described with previously characterized antibodies. In fact, even though the staining was weaker than in tumor tissues, all tissues were found to be positive, at least in microvessels, except for normal breast. Moreover, in some tissues (glands and reproductive tract) a positive reaction was observed in the stroma. Since endoglin has been proposed as a possible target for antiangiogenic therapy in tumor patients and our data demonstrate a sizable amount of endoglin in normal vessels and stroma, its clinical use should be carefully reevaluated.

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Endoglin overexpression modulates cellular morphology, migration, and adhesion of mouse fibroblasts

Cited by 89 publications

References 63 publications

Over expression of endoglin in human prostate cancer suppresses cell detachment, migration and invasion

Over expression of endoglin in human prostate cancer suppresses cell detachment, migration and invasion

PRH/HHex inhibits the migration of breast and prostate epithelial cells through direct transcriptional regulation of Endoglin

Lack of specificity of endoglin expression for tumor blood vessels

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