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Modeling Tumor Development: the Role of L1
Author(s) -
Brady Owen Adam,
Yang Muhua,
Galileo Deni S.
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.1029.3
Subject(s) - ectodomain , cell migration , microbiology and biotechnology , autocrine signalling , paracrine signalling , integrin , biology , transfection , filopodia , neural cell adhesion molecule , cell adhesion , cell , cancer cell , glioma , receptor , cell culture , cancer research , biochemistry , cancer , actin , genetics
L1 is a membrane‐bound neural cell adhesion protein involved in the development of the nervous system. However, L1 has been implicated in mediating some of the invasive properties of several cancers including gliomas and breast cancers when proteolyzed to create a soluble ectodomain, which then binds to cell surface integrin receptors in an autocrine/paracrine manner. L1 has also been shown to rescue cancerous cells from apoptosis. It was hypothesized that polyclonal antibodies raised against a 15 amino acid peptide corresponding to a critical integrin binding region of human L1 would slow the migration of rat 9L/LacZ and human T98 G glioma cells in vitro , whereas the peptide alone would stimulate migration. Incubation of cells in the peptide decreased cellular migration, possibly due to competitive inhibition. The effects of the antibody on cell migration were inconclusive. Quail QT6 cells have been stably transfected with an L1 ectodomain‐Fc fusion protein (L1‐Fc) designed to be secreted into the media. Once purified, it will be applied to 9L/LacZ and T98 G cells and analyzed using automated time‐lapse microscopy. Additionally, glioma cell migration will be analyzed while on top of QT6 cells secreting L1‐Fc. Both conditions are hypothesized to increase the migration rates of these cell lines by mimicking the activity of endogenous L1 ectodomains. Supported by HHMI and INBRE.