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Elevated expression of endoglin, a component of the TGF‐β‐receptor complex, correlates with proliferation of tumor endothelial cells
Author(s) -
Miller Daniel W.,
Graulich Wolff,
Karges Bernadett,
Stahl Sabine,
Ernst Michael,
Ramaswamy Annette,
Sedlacek H.Harald,
Müller Rolf,
Adamkiewicz Jürgen
Publication year - 1999
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/(sici)1097-0215(19990517)81:4<568::aid-ijc11>3.0.co;2-x
Subject(s) - endoglin , immunohistochemistry , endothelial stem cell , cancer research , biology , receptor , transforming growth factor , cell growth , microbiology and biotechnology , immunology , genetics , cd34 , stem cell , in vitro
Endoglin/CD105 is a membrane protein involved in the TGF‐β receptor signalling pathway. Endoglin expression has been reported to be selective for a few cell types, in particular endothelial cells, although a number of conflicting reports have been published. In this study, we performed a detailed analysis of endoglin expression in human lung tumors and different tumor and endothelial cell lines, employing reverse‐transcriptase‐polymerase‐chain reaction as well as immunoblotting and immunohistochemistry using verified antibodies to endoglin. Our data show a clearly preferential expression of both endoglin mRNA and protein in endothelial cells. In tumors, endoglin expression was strongly elevated in the angiogenic endothelium at the tumor edges. In agreement with this observation, we find a clear correlation between endoglin expression and markers of proliferation, such as cyclin A and Ki‐67, suggesting that endoglin expression is linked to cell‐cycle regulation. These findings not only resolve some of the discrepancies in the literature, but also provide the basis for further applications making use of its selective localization and expression in the tumor vasculature. Int. J. Cancer 81:568–572, 1999. © 1999 Wiley‐Liss, Inc.

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