Expression and structural features of endoglin (CD105), a transforming growth factor β1 and β3 binding protein, in human melanoma

Altomonte, Maresa; Montagner, R.; Fonsatti, Ester; Colizzi, Francesca; Cattarossi, Ilaria; Braşoveanu, Lorelei Irina; Nicotra, Maria Rita; Cattelan, Anna María; Natali, Pier Giorgio; Maio, Michele

doi:10.1038/bjc.1996.593

Cited by 58 publications

(41 citation statements)

References 24 publications

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“…Indeed, and although truly 'normal' prostates from young men (autopsy, organ donors) could not be processed as whole-mounts in our setting, the lack of staining in the normal/benign epithelium in the studied patient's population (91% of cases) is in agreement with the literature. 12,[14][15][16][17][18] On the other hand, observations on high endoglin-staining in epithelial cells of PIN lesions and tumors in these whole-mount sections, and often more intense in PIN than cancer within a specimen, are 20 While this may suggest a link with early phases of the disease, studies are underway to establish whether endoglin expression in prostate tumor cells is associated progression. Notably, in vitro studies in prostatic carcinoma cell lines indicate that endoglin exerts a function of its own linked to adhesion and migration/invasion.…”

Section: Discussionmentioning

confidence: 99%

“…15 On the other hand, endoglin is rarely detected in normal epitheliums, with the exception of the glomerular mesangium in human kidneys 16 and melanocytes. 17 Of particular interest is that in addition to leukemic cells, 1 endoglin is expressed in cancers, namely melanoma 17 and ovarian carcinoma. 18 Altogether endoglin expression levels in blood vessels but also in stromal and to some extent epithelial cells, seem to be altered according to diseases in diverse human tissues.…”

Section: Introductionmentioning

confidence: 99%

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Whole-mount prostate sections reveal differential endoglin expression in stromal, epithelial, and endothelial cells with the development of prostate cancer

Kassouf

Ismail

Aprikian

et al. 2004

Prostate Cancer Prostatic Dis

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Endoglin is a nonsignaling receptor for transforming growth factor that contributes to the action of this growth factor in diverse cell types. It may also exhibit a function of its own. Endoglin levels vary with disease states and is a marker of new blood vessels. We studied endoglin expression in whole-mount prostate sections from 64 patients with localized prostate cancer, assessing reactivity in the epithelium, the stroma, and blood vessels. Cells in normal/benign acini were negative but significantly immunoreactive (Po0.001) in both prostatic intraepithelial neoplasia (PIN; 52% of cases) and malignant areas (77% of cases). In tumors, this involved less than 25% of malignant cells in 59% of specimens. The endoglin-stained stroma was detected mainly in areas surrounding PIN acini and tumors. Endoglin antibodies detected more microvessels than von Willebrand Factor antibodies in all prostatic areas (Po0.01). In addition, the number of microvessels increased with the development of cancer and correlated with Gleason score (Po0.01). Changes in endoglin expression in PIN and malignant cells, the surrounding stroma, and related blood vessels, suggest that endoglin function may be altered in prostate cancer.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Whole-mount prostate sections reveal differential endoglin expression in stromal, epithelial, and endothelial cells with the development of prostate cancer

Kassouf

Ismail

Aprikian

et al. 2004

Prostate Cancer Prostatic Dis

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“…TGFb is known to modulate cell adhesion and motility in a variety of cell types (Albo et al, 1997;Cai et al, 2000;Loganadane et al, 1999;Merzak et al, 1994;Teti et al, 1997), including prostate (Festuccia et al, 1999). Finally, endoglin contains the tripeptide motif, arg-glyasp (RGD) in its extracellular domain (Altomonte et al, 1996;Gougos and Letarte, 1990). The RGD motif is associated with the extracellular matrix protein, fibronectin, and is the ligand by which fibronectin binds integrins (including b1-integrin) (Witkowski et al, 1993).…”

Section: Introductionmentioning

confidence: 99%

“…Endoglin has homology to transforming growth factor b (TGFb) receptor type III, will bind TGFb (Cheifetz et al, 1992), and modulates TGFb signaling in several systems, inhibiting TGFb action in some (Lastres et al, 1996;Letamendia et al, 1998), augmenting it in others (Altomonte et al, 1996). TGFb is known to modulate cell adhesion and motility in a variety of cell types (Albo et al, 1997;Cai et al, 2000;Loganadane et al, 1999;Merzak et al, 1994;Teti et al, 1997), including prostate (Festuccia et al, 1999).…”

Section: Introductionmentioning

confidence: 99%

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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“…MAb and conventional antisera The anti-ICAM-l MAb 84H10, the anti-LFA-3 MAb TS2/9 and the anti-endoglin MAb MAEND3 were developed and characterized as described previously (Sanchez-Madrid et al, 1982;Makgoba et al, 1988;Altomonte et al, 1996). The anti-HLA class I MAb W6/32 was purchased from ATCC.…”

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confidence: 99%

Tumour-derived interleukin 1α (IL-1α) up-regulates the release of soluble intercellular adhesion molecule-1 (sICAM-1) by endothelial cells

Fonsatti

Altomonte²,

Coral³

et al. 1997

Br J Cancer

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Summary Levels of circulating soluble intercellular adhesion molecule-1 (sICAM-1) are elevated in patients affected by solid malignancies; however, the cellular sources generating high levels of sICAM-1 remain to be characterized. Using conditioned media (CM) from seven ICAM-1-positive or -negative neoplastic cells, we demonstrate that tumour-derived interleukin 1a (IL-1 a) significantly (P < 0.05) up-regulates the release of sICAM-1 by human umbilical vein endothelial cells. The intensity of the effect correlated with the amounts of IL-la detectable in CM. Levels of ICAM-1 mRNA were also up-regulated by tumour-secreted IL-i a. The up-regulation of the shedding of sICAM-1 and of its expression at protein and mRNA level were completely reversed by the addition of anti-IL-i a neutralizing antibodies. Consistent with the in vitro data, tumour endothelia were strongly stained for ICAM-1 compared with autologous normal tissue endothelia. Taken altogether, our observations reveal an IL-la-mediated tumour-endothelium relationship sustaining the shedding of sICAM-1 by endothelial cells. This is a general phenomenon in solid malignancies that correlates with the ability of neoplastic cells to secrete IL-1a rather than with their expression of ICAM-1 and/or histological origin. sICAM-1 has been previously shown to inhibit LFA-1/ICAM-1-mediated cell-cell interactions; therefore, the ability of neoplastic cells to secrete IL-1a is likely to represent a mechanism for their escape from immune interaction.

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Expression and structural features of endoglin (CD105), a transforming growth factor β1 and β3 binding protein, in human melanoma

Cited by 58 publications

References 24 publications

Whole-mount prostate sections reveal differential endoglin expression in stromal, epithelial, and endothelial cells with the development of prostate cancer

Whole-mount prostate sections reveal differential endoglin expression in stromal, epithelial, and endothelial cells with the development of prostate cancer

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

Tumour-derived interleukin 1α (IL-1α) up-regulates the release of soluble intercellular adhesion molecule-1 (sICAM-1) by endothelial cells

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