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    Competing autocrine pathways involving alternative neuropilin-1 ligands regulate chemotaxis of carcinoma cells

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    Authors
    Bachelder, Robin E.
    Lipscomb, Elizabeth A.
    Lin, Xuena
    Wendt, Melissa A.
    Chadborn, Neil H.
    Eickholt, Britta J.
    Mercurio, Arthur M.
    UMass Chan Affiliations
    Department of Cancer Biology
    Document Type
    Journal Article
    Publication Date
    2003-09-23
    Keywords
    Breast Neoplasms
    Carcinoma
    Chemotaxis
    Endothelial Growth Factors
    Humans
    Intercellular Signaling Peptides and Proteins
    Ligands
    Lymphokines
    Nerve Tissue Proteins
    Neuropilin-1
    RNA Interference
    RNA, Messenger
    Receptors, Cell Surface
    Semaphorin-3A
    Transfection
    Vascular Endothelial Growth Factor A
    Vascular Endothelial Growth Factors
    Cancer Biology
    Neoplasms
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    Link to Full Text
    http://cancerres.aacrjournals.org/content/63/17/5230.full.pdf+html
    Abstract
    Neuropilin-1 (NP1), in conjunction with plexins, promotes axon repulsion by binding to semaphorin 3A (SEMA3A). Although NP1 is expressed in carcinoma cells, its functions have remained elusive, and neither SEMA3A nor plexin expression has been explored in cancer. Here we provide evidence that breast carcinoma cells support an autocrine pathway involving SEMA3A, plexin-A1, and NP1 that impedes their ability to chemotax. Reducing SEMA3A or NP1 expression by RNA interference or inhibiting plexin-A1 signaling enhanced migration. Conversely, expression of constitutively active plexin-A1 impaired chemotaxis. The paradox of how breast carcinoma cells expressing these endogenous chemotaxis inhibitors are able to migrate is explained by their expression of vascular endothelial growth factor (VEGF), a NP1 ligand that competes with SEMA3A for receptor binding. Finally, we establish that the ratio of endogenous VEGF and SEMA3A concentrations in carcinoma cells determines their chemotactic rate. Our findings lead to the surprising conclusion that opposing autocrine loops involving NP1 regulate the chemotaxis of breast carcinoma cells. Moreover, our data indicate a novel autocrine function for VEGF in chemotaxis.
    Source
    Cancer Res. 2003 Sep 1;63(17):5230-3.
    Permanent Link to this Item
    http://hdl.handle.net/20.500.14038/26251
    PubMed ID
    14500350
    Related Resources
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    UMass Chan Faculty and Researcher Publications

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