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  LGALS3BP, lectin galactoside-binding soluble 3 binding protein, induces vascular endothelial growth factor in human breast cancer cells and promotes angiogenesis

Piccolo, E., Tinari, N., Semeraro, D., Traini, S., Fichera, I., Cumashi, A., et al. (2013). LGALS3BP, lectin galactoside-binding soluble 3 binding protein, induces vascular endothelial growth factor in human breast cancer cells and promotes angiogenesis. JOURNAL OF MOLECULAR MEDICINE-JMM, 91(1), 83-94. doi:10.1007/s00109-012-0936-6.

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Piccolo, Enza1, Autor
Tinari, Nicola1, Autor
Semeraro, Daniela1, Autor
Traini, Sara1, Autor
Fichera, Imma1, Autor
Cumashi, Albana1, Autor
La Sorda, Rossana1, Autor
Spinella, Francesca1, Autor
Bagnato, Anna1, Autor
Lattanzio, Rossano1, Autor
D'Egidio, Maurizia1, Autor
Di Risio, Annalisa1, Autor
Stampolidis, Pavlos2, Autor           
Piantelli, Mauro1, Autor
Natoli, Clara1, Autor
Ullrich, Axel2, Autor           
Iacobelli, Stefano1, Autor
Affiliations:
1external, ou_persistent22              
2Ullrich, Axel / Molecular Biology, Max Planck Institute of Biochemistry, Max Planck Society, ou_1565172              

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Schlagwörter: CYSTEINE-RICH DOMAIN; 90K MAC-2 BP; TUMOR ANGIOGENESIS; SIGNALING PATHWAY; ANTIGEN 90K; EXPRESSION; SURVIVAL; METASTASIS; ANTIBODY; FAMILYAngiogenesis; VEGF; LGALS3BP; Extracellular matrix; Galectin-3;
 Zusammenfassung: Elevated serum or tissue levels of lectin galactoside-binding soluble 3 binding protein (LGALS3BP) have been associated with short survival and development of metastasis in a variety of human cancers. However, the role of LGALS3BP, particularly in the context of tumor-host relationships, is still missing. Here, we show that LGALS3BP knockdown in MDA-MB-231 human breast cancer cells leads to a decreased adhesion to fibronectin, a reduced transendothelial migration and, more importantly, a reduced expression of vascular endothelial growth factor (VEGF). Production of VEGF, that was restored by exposure of silenced cells to recombinant LGALS3BP, required an intact PI3k/Akt signaling. Furthermore, we show that LGALS3BP was able to directly stimulate HUVEC tubulogenesis in a VEGF-independent, galectin-3-dependent manner. Immunohistochemical analysis of human breast cancer tissues revealed a correlation among LGALS3BP expression, VEGF expression, and blood vessel density. We propose that in addition to its prometastatic role, LGALS3BP secreted by breast cancer cells functions critically as a pro-angiogenic factor through a dual mechanism, i.e by induction of tumor VEGF and stimulation of endothelial cell tubulogenesis.

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Sprache(n): eng - English
 Datum: 2013-01
 Publikationsstatus: Erschienen
 Seiten: 12
 Ort, Verlag, Ausgabe: -
 Inhaltsverzeichnis: -
 Art der Begutachtung: Expertenbegutachtung
 Identifikatoren: ISI: 000313077000009
DOI: 10.1007/s00109-012-0936-6
 Art des Abschluß: -

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Titel: JOURNAL OF MOLECULAR MEDICINE-JMM
Genre der Quelle: Zeitschrift
 Urheber:
Affiliations:
Ort, Verlag, Ausgabe: 233 SPRING ST, NEW YORK, NY 10013 USA : SPRINGER
Seiten: - Band / Heft: 91 (1) Artikelnummer: - Start- / Endseite: 83 - 94 Identifikator: ISSN: 0946-2716