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Vascular endothelial growth factor-D is a survival factor for human breast carcinoma cells

✍ Scribed by Manabu Akahane; Takemi Akahane; Shannon L. Matheny; Amy Shah; Eijiro Okajima; Unnur P. Thorgeirsson

Publisher
John Wiley and Sons
Year
2005
Tongue
French
Weight
564 KB
Volume
118
Category
Article
ISSN
0020-7136

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✦ Synopsis

Abstract

Vascular endothelial growth factor‐D (VEGF‐D) stimulates growth of vascular and lymphatic endothelial cells by signaling through the tyrosine kinase receptors KDR (VEGFR‐2) and Flt‐4 (VEGFR‐3). In the present study, we examined the effects of VEGF‐D on apoptosis in human MCF‐7 and MDA‐MB‐231 breast carcinoma cells. Because VEGF‐D was not expressed constitutively in vitro, stable VEGF‐D transfectants were produced. The VEGF‐D‐expressing MCF‐7 and MDA‐MB‐231 lines displayed resistance to apoptosis induced by hypoxia, staurosporin and cycloheximide. Increased Bcl‐2 expression, decreased homogenous caspase activities and inhibition of poly(ADP‐ribose) polymerase cleavage were associated with inhibition of apoptosis in VEGF‐D‐expressing clones. Also, caspase‐3 activation was suppressed in the VEGF‐D expressing MDA‐MB‐231 clone. The antiapoptotic effect of VEGF‐D in vitro was recapitulated in vivo using VEGF‐D‐expressing MDA‐MB‐231 xenografts. The lack of VEGFR‐2 protein expression by Western blot and ineffectiveness of a neutralizing VEGFR‐2 antibody in eliminating the antiapoptotic effects of VEGF‐D suggest a different and yet unknown signaling mechanism. Our findings indicate that VEGF‐D has a novel function as a survival factor of breast carcinoma cells in addition to its established functions as an angiogenic and lymphangiogenic factor. © 2005 Wiley‐Liss, Inc.

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