Abstract
Two human mammary carcinoma cell variants, MCF-7/AZ and MCF-7/6, show the same composition in their glycosphingolipid-enriched microdomain (GEM) with regard to globo-series structures Gb3, Gb4, Gb5, monosialyl-Gb5, GM2, and cSrc and FAK. Both variants are non-invasive into collagen gel layer, and showed similar motility in wound migration assay. Whereas invasiveness and motility of MCF-7/AZ cells were enhanced greatly by treatment with mAb RM1 directed to monosialyl-Gb5, the same RM1 treatment had no effect on MCF-7/6. cSrc and FAK of MCF-7/AZ, but not MCF-7/6, were activated by RM1 treatment. Thus, malignancy of MCF-7 is highly dependent on monosialyl-Gb5, and its activation of cSrc and FAK in GEM.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Antibodies, Monoclonal
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Antigens, CD / biosynthesis
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Cell Line
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Cell Movement
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Chromatography, Thin Layer
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Collagen / chemistry
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Collagen / metabolism
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Enzyme Activation
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Focal Adhesion Kinase 1
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Focal Adhesion Protein-Tyrosine Kinases
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Humans
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Immunoglobulin M / metabolism
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Membrane Glycoproteins / biosynthesis
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Microscopy, Fluorescence
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Neoplasm Invasiveness
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Protein Structure, Tertiary
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Protein-Tyrosine Kinases / metabolism*
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Signal Transduction
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Sphingolipids / metabolism*
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Tetraspanin 29
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Time Factors
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Tumor Cells, Cultured
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Wound Healing
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src-Family Kinases / metabolism*
Substances
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Antibodies, Monoclonal
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Antigens, CD
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CD9 protein, human
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Immunoglobulin M
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Membrane Glycoproteins
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Sphingolipids
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Tetraspanin 29
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Collagen
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Protein-Tyrosine Kinases
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Focal Adhesion Kinase 1
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Focal Adhesion Protein-Tyrosine Kinases
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PTK2 protein, human
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src-Family Kinases