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Vasohibin‐1 expression inhibits advancement of ovarian cancer producing various angiogenic factors
Author(s) -
Takahashi Yoshifumi,
Saga Yasushi,
Koyanagi Takahiro,
Takei Yuji,
Machida Shizuo,
Taneichi Akiyo,
Mizukami Hiroaki,
Sato Yasufumi,
Matsubara Shigeki,
Fujiwara Hiroyuki
Publication year - 2016
Publication title -
cancer science
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.035
H-Index - 141
eISSN - 1349-7006
pISSN - 1347-9032
DOI - 10.1111/cas.12911
Subject(s) - vascular endothelial growth factor , cancer research , angiogenesis , ovarian cancer , growth factor , platelet derived growth factor receptor , cell culture , basic fibroblast growth factor , biology , vascular endothelial growth factor a , transfection , cancer cell , cancer , endocrinology , medicine , vegf receptors , receptor , genetics
Vasohibin‐1 ( VASH 1) is a negative feedback regulator of angiogenesis, the first to be discovered, and was identified in vascular endothelial growth factor ( VEGF )‐stimulated vascular endothelial cells. Vasohibin‐1 inhibits abnormal vascularization induced by various angiogenic factors including fibroblast growth factor and platelet‐derived growth factor ( PDGF ), in addition to VEGF . By focusing on this characteristic of VASH 1, we investigated the antitumor effects of VASH 1 expression on ovarian cancer cells that produce different angiogenic factors. By using a high VEGF ‐producing ovarian cancer cell line, SHIN ‐3, and a high PDGF ‐producing ovarian cancer cell line, KOC ‐2S, the cells were transfected with either a VEGF antagonist, soluble VEGF receptor‐1 ( sVEGFR ‐1, or sF lt‐1), or VASH 1 genes to establish their respective cellular expression. The characteristics of these transfectants were compared with controls. We previously reported that the expression of sF lt‐1 inhibited tumor vascularization and growth of high VEGF ‐producing ovarian cancer cells, reduced peritoneal dissemination and ascites development, and prolonged the survival time of the host. However, in the current study, the expression of sF lt‐1 had no such effect on the high PDGF ‐producing ovarian cancer cells used here, whereas VASH 1 expression inhibited tumor vascularization and growth, not only in high VEGF ‐producing cells, but also in high PDGF ‐producing cells, reduced their peritoneal dissemination and ascites, and prolonged the survival time of the host. These results suggest that VASH 1 is an effective treatment for ovarian cancer cells that produce different angiogenic factors.

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