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Título: | VEGF/VEGFR2 interaction down-regulates matrix metalloproteinase–9 via STAT1 activation and inhibits B chronic lymphocytic leukemia cell migration |
Autor: | Ugarte-Berzal, Estefanía CSIC ORCID; Redondo-Muñoz, Javier CSIC ORCID ; Eroles, Pilar; Hernández del Cerro, Mercedes CSIC; García-Marco, José A.; Terol, María José; García-Pardo, Angeles CSIC ORCID | Palabras clave: | Lymphoid Neoplasia Lymphocytic leukemia |
Fecha de publicación: | 28-ene-2010 | Editor: | American Society of Hematology | Citación: | Blood, 115:846-849 (2010 ) | Resumen: | B-cell chronic lymphocytic leukemia (B-CLL) migration involves several molecules, including matrix metalloproteinase–9 (MMP-9) and vascular endothelial growth factor (VEGF). We have studied whether VEGF regulates MMP-9. VEGF significantly reduced MMP-9 protein expression in a dose-dependent manner, measured by gelatin zymography. Blocking the VEGFR2 receptor restored MMP-9 levels, implicating this receptor in the observed effect. Down-regulation of MMP-9 by VEGF resulted in significant inhibition of B-CLL cell migration through Matrigel or human umbilical vein endothelial cells, confirming the crucial role of MMP-9 in these processes. Reverse-transcription polymerase chain reaction analyses revealed that VEGF regulated MMP-9 at the transcriptional level. Indeed, VEGF induced STAT1 tyrosine phosphorylation, and this was blocked by inhibiting VEGFR2. STAT1 was responsible for MMP-9 down-regulation, as STAT1 gene silencing restored MMP-9 production and B-CLL cell migration in the presence of VEGF. Thus, the levels of VEGF and MMP-9 influence B-CLL cell expansion and both molecules could constitute therapeutic targets for this disease. | Descripción: | Brief Report. Artículo breve. | Versión del editor: | http://bloodjournal.hematologylibrary.org/content/115/4/846.full.pdf | URI: | http://hdl.handle.net/10261/39606 | DOI: | 10.1182/blood-2009-08-239426 | ISSN: | 0006-4971 | E-ISSN: | 1528-0020 |
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