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Neuropilin-1 promotes unlimited growth of ovarian cancer by evading contact inhibition.

Abstract：

OBJECTIVE:Neuropilin-1 (NRP-1) is a receptor for both semaphorin and vascular endothelial growth factor and is up-regulated in a variety of human cancers. While there are some reports of NRP-1 expression in ovarian neoplasm, those results differ in pattern of its expression and its role in ovarian cancer is still unclear. We sought to investigate the expression pattern and role of NRP-1 in ovarian cancer. METHODS:NRP-1 expression was analyzed with eighty-seven ovarian tissue samples by immunohistochemistry and four ovarian cell lines by quantitative RT-PCR and Western blotting. To detect its molecular role in ovarian cancer, WST-1 assay, invasion assay and soft agar assay were performed with or without NRP-1 suppression by the introduction of short hairpin RNAs. RESULTS:NRP-1 expression was found to be enhanced in ovarian cancer compared with ovarian surface epithelium (OSE), benign adenoma and tumors of low malignant potential. In vitro, NRP-1 expression was augmented threefold during malignant transformation of OSE cells with oncogene ras, suggesting an association between NRP-1 and oncogenesis. Suppression of NRP-1 reduced cell proliferation in a dense state, indicating that persistently high expression of NRP-1 in ovarian cancer enhances proliferation through evasion of contact inhibition. Suppression of NRP-1 also decreased cell growth in soft agar and invasion to the extracellular matrix in vitro. CONCLUSIONS:These results suggest that NRP-1 is not only associated with oncogenesis, but also with ovarian cancer malignancy, and this molecule is a targeting candidate for the treatment of ovarian malignancies.

journal_name

Gynecol Oncol

journal_title

Gynecologic oncology

authors

Baba T,Kariya M,Higuchi T,Mandai M,Matsumura N,Kondoh E,Miyanishi M,Fukuhara K,Takakura K,Fujii S

doi

10.1016/j.ygyno.2007.02.005

subject

Has Abstract

pub_date

2007-06-01 00:00:00

pages

703-11

issue

3

eissn

0090-8258

issn

1095-6859

pii

S0090-8258(07)00126-6

journal_volume

105

pub_type

杂志文章

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