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  • 1
    Keywords: RECEPTOR ; ANGIOGENESIS ; CANCER ; CANCER CELLS ; CELLS ; EXPRESSION ; GROWTH ; tumor ; TUMOR-CELLS ; carcinoma ; ENDOTHELIAL GROWTH-FACTOR ; Germany ; human ; PATHWAY ; SYSTEM ; PROTEIN ; TISSUE ; TUMORS ; LINES ; PATIENT ; COMPLEX ; COMPLEXES ; MARKER ; prognosis ; TISSUES ; BINDING ; CELL-LINES ; SIGNAL ; NERVOUS-SYSTEM ; PROGRESSION ; ovarian cancer ; OVARIAN-CANCER ; CELL-LINE ; FUSION ; LINE ; CANCER-CELLS ; ADHESION ; INTEGRIN ; CARCINOMAS ; RT-PCR ; L1 ; NEURITE OUTGROWTH ; ADHESION MOLECULE ; L1 adhesion molecule ; ovarian carcinoma ; OVEREXPRESSION ; cell lines ; TUMOR CELLS ; PERMEABILITY ; RE ; TUMOR-GROWTH ; cell adhesion ; LEVEL ; TUMOR-CELL ; ADHESION MOLECULE L1 ; OVARIAN CARCINOMAS ; function ; SIGNALS ; OVARIAN ; VARIETIES ; VASCULAR-PERMEABILITY ; heterophilic binding ; mesothelial cells ; MOUSE LEUKOCYTES ; neuropilin-1 ; SEMAPHORIN-III
    Abstract: The progression of ovarian cancer is driven by a variety of cellular factors that are incompletely understood. Binding of tumor cells to normal cells and to soluble factors influence tumor growth, angiogenesis and the stimulation of vascular permeability leading to ascites production. L1 adhesion molecule is overexpressed in ovarian carcinoma and is associated with bad prognosis. One receptor for L1 is Neuropilin-1 (NRP-1) that is also known as a receptor for VEGF(165). In the nervous system a complex of NRP-1 and L1 transmits signals by the neurorepellant Sem3A that is critical for the control of neurite outgrowth. NRP-1 has also been detected in human carcinomas but its function remains unknown. Here, we have examined NRP-1 expression in ovarian carcinoma cell lines and tissue. We report that little NRP-1 protein was detected in primary ovarian carcinoma tissues or established cell lines although mRNA for soluble and transmembrane NRP-1 were detected by RT-PCR. Instead, we observed strong expression of NRP-1 in mesothelial cells, which form the lining of the peritoneum. NRP-1 could serve as an isolation marker for primary mesothelial cells present in ascites fluid. We demonstrate that ovarian cancer cells expressing L1 can bind to NRP-1 overexpressing cells and mesothelial cells. Likewise, soluble L1 isolated from ascites of patients or produced as a fusion protein could bind to NRP-1 overexpressing cells and a direct interaction was demonstrated at the protein level. These findings suggest that L1 can support the binding of ovarian carcinoma cells to mesothelial cells via NRP-1. The L1-NRP-1 binding pathway could contribute to the growth of ovarian carcinomas and to reciprocal signalling between mesothelial cells and tumors. (c) 2005 Elsevier Ireland Ltd. All rights reserved
    Type of Publication: Journal article published
    PubMed ID: 16377081
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  • 2
    Keywords: CELLS ; EXPRESSION ; GROWTH ; tumor ; carcinoma ; Germany ; KINASE ; PATHWAY ; GENE ; GENE-EXPRESSION ; PROTEIN ; PROTEINS ; TISSUE ; TUMORS ; LINES ; MICE ; gene transfer ; GENE-TRANSFER ; ACTIVATION ; prognosis ; CELL-LINES ; VARIANTS ; MOLECULE ; PROGRESSION ; gene expression ; TUMOR PROGRESSION ; METASTASIS ; LINE ; EXTRACELLULAR-MATRIX ; BETA ; ADHESION ; MIGRATION ; INTEGRIN ; CARCINOMAS ; L1 ; ADHESION MOLECULE ; ovarian carcinoma ; OVEREXPRESSION ; cell lines ; CELL-MIGRATION ; MORPHOGENESIS ; MATRIX ; RE ; TUMOR-GROWTH ; extracellular matrix ; cell adhesion ; cell migration ; CANCER PROGRESSION ; PROFILES ; ERK ; EPITHELIUM ; ADHESION MOLECULE L1 ; CD171 ; CUTANEOUS MALIGNANT-MELANOMA ; VITRONECTIN
    Abstract: L1 is a neural cell adhesion molecule involved in cell migration, axon growth and guidance. Recent data have shown that L1 is overexpressed in ovarian and endometrial tumors and is associated with bad prognosis. How L1 promotes tumor progression is presently unknown. Here we show that L1 expression is predominantly confined to the invasive front of ovarian carcinomas. Overexpression of L1 in carcinoma cell lines by adenovirus-mediated gene transfer enhanced the haptotactic cell migration on extracellular matrix proteins. Expression of L1 augmented tumor growth of carcinomas xenografted in nonobese diabetic/severe combined immunodeficient mice (NOD/SCID). A recent report has demonstrated L1-dependent upregulation of P3 integrin involving activation of the extracellular signal-regulated kinase (erk) pathway. We find that L1 and P3 integrin are not coexpressed in ovarian carcinoma tissues. Overexpression of L1 did not upregulate P3 integrin in ovarian carcinoma cell lines but could do so in HEK293 cells. Our results suggest that L1 could drive progression by enhancing cell migration and tumor growth but that L1 dependent and erk-regulated gene expression requires cell-type specific elements. © 2005 Wiley-Liss, Inc
    Type of Publication: Journal article published
    PubMed ID: 15704102
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