Journal
GYNECOLOGIC ONCOLOGY
Volume 108, Issue 2, Pages 361-369Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.ygyno.2007.10.027
Keywords
ovarian cancer; LPA; soluble E-cadherin; invasion; uPA
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Objectives. To evaluate the role of LPA in regulating E-cadherin cell surface expression, adhesion, and invasion in epithelial ovarian carcinoma (EOC) cells. Methods. E-cadherin mRNA expression in OVCA429 and IOSE-29 cells was evaluated by real-time RT-PCR. Immunofluorescence and Western blot analysis were performed to determine cell surface expression and shedding of E-cadherin 80-kDa soluble fragment by LPA. Kinetics of LPA-induced uPA activity was followed with a colorimetric enzymatic assay. Invasion assays were performed in a modified Boyden chamber where cells were allowed to migrate to the bottom compartment through a porous filter coated with collagen. Additionally we measured the 80kDa form from the ascites of women with stage III/IV EOC. Results. LPA induces E-cadherin shedding of a soluble 80-kDa fragment. We found that this process is mediated by the uPA proteolytic cascade. High levels of soluble E-cadherin were found in the ascites from women with advanced stage EOC. LPA and a soluble recombinant Ecadherin-Fc chimera promotes invasion of OVCA429 cells. Conclusions. LPA induces shedding of an 80-kDa E-cadherin-soluble fragment in an uPA-dependent manner and promotes in vitro invasion. Nigh levels of soluble E-cadherin in malignant ascites may also affect ovarian metastasis. (C) 2007 Elsevier Inc. All rights reserved.
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