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The expression and characterization of endoglin in uterine leiomyosarcoma

Authors :
Eiko Yamamoto
Takeshi Senga
Tomokazu Umezu
Hiroko Mitsui
Tomomi Kotani
Kiyosumi Shibata
Shiro Suzuki
Yukio Mano
Mika Mizuno
Fumitaka Kikkawa
Hiroaki Kajiyama
Source :
Clinical & Experimental Metastasis. 30:731-740
Publication Year :
2013
Publisher :
Springer Science and Business Media LLC, 2013.

Abstract

Endoglin (CD105), an accessory receptor of transforming growth factor-β, is expressed in vascular endothelial cells. Recently, it was reported that endoglin expression was significantly associated with poorer survival in several cancers. In this study, we evaluated the role of endoglin in uterine leiomyosarcoma. We examined the expression of endoglin in 22 uterine leiomyosarcomas and the association between their expression and the outcome. Additionally, to evaluate the function of endoglin, we used SKN cells, a human uterine leiomyosarcoma cell line. We generated SKN cells stably transfected with plasmids encompassing shRNA targeting endoglin (shEng cells), and compared the ability of proliferation, migration, and invasion to control shRNA-transfected cells (shCon cells). We compared the level of VEGF and matrix metalloproteinases (MMP) in culture supernatants of shEndoglin and shControl cells. Nine patients were endoglin-positive and 13 patients were -negative. The endoglin-positive group had a significantly poorer overall survival and progression-free survival than the endoglin-negative group. In an in vitro study, there was no difference in cell proliferation between shEng and shCon cells. On the other hand, shEng cells showed a lower ability for migration and invasion than shControl cells. The activity of MMP-9 and VEGF level in the supernatant from shEng cells were lower than in shCon cells. In uterine leiomyosarcoma, endoglin expression was associated with a poor prognosis. It was suggested that endoglin up-regulated invasion and VEGF secretion. The investigation of endoglin may lead to a new strategy in uterine leiomyosarcoma therapy.

Details

ISSN :
15737276 and 02620898
Volume :
30
Database :
OpenAIRE
Journal :
Clinical & Experimental Metastasis
Accession number :
edsair.doi.dedup.....326c9aaec621357ffbf0cc92d4eb4a0b