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  • Articles: DFG German National Licenses  (2)
  • Cell & Developmental Biology  (1)
  • Glycosaminoglycan  (1)
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  • Articles: DFG German National Licenses  (2)
Material
Years
  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Journal of cancer research and clinical oncology 115 (1989), S. 554-557 
    ISSN: 1432-1335
    Keywords: Human melanoma ; Metastasis ; Glycosaminoglycan ; Xenograft
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Two human melanoma xenografts were compared with respect to their in vivo growth and metastatic potentials as well as glycosaminoglycan patterns. The less differentiated HT 168 tumor showed faster growth at primary sites and a more pronounced capacity for metastasis into the liver. Although chondroitin sulfate was the dominant glycosaminoglycan subtype in both tumors, the more invasive xenograft had a higher heparan sulfate/chondroitin sulfate (HS/CS) ratio. We suggest that tumor progression is influenced by this ratio in this human melanoma system.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    New York, NY : Wiley-Blackwell
    Cell Motility and the Cytoskeleton 26 (1993), S. 49-65 
    ISSN: 0886-1544
    Keywords: fatty acid ; MHC ; MLC ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: The fatty acid 12(S)-HETE may be a new second messenger capable of activating PKC. In tumor cells 12(S)-HETE stimulates cytoskeleton-dependent cellular responses such as adhesion and spreading. Analysis of 12(S)-HETE effects on B16a melanoma cell cytoskeleton revealed reversible rearrangement of microtubules, microfilaments, the actin-binding proteins, vinculin, myosin heavy (MHC) and light chains (MLC), as well as bundling of vimentin intermediate filaments. The alterations in microfilaments and intermediate filaments occurred very rapidly, i.e., 5 min after exposure of tumor cells to 12(S)-HETE. The 12(S)-HETE-induced cytoskeletal alterations were accompanied by centrifugal organelle-translocation. Interestingly, MLC exhibited clear association with the cytoplasmic organelles. Biochemical analysis of the 12(S)-HETE effect indicated a PKC-mediated reversible hyperphosphorylation of MLC, vimentin, and a 130 kD cytoskeletal-associated protein. Optimal effects were obtained after 5 min treatment with 12(S)-HETE at 0.1 μM concentration. 12(S)-HETE pretreatment induced tumor cell spreading on a fibronectin matrix which required the intactness of all three major cytoskeletal components. The spreading process was dependent upon the activity of PKC. Our data suggest that 12(S)-HETE is a physiological stimulant of PKC. Further, it induces rearrangement of the cytoskeleton of tumor cells in interphase resulting in the stimulation of cytoskeleton-dependent cell activity such as spreading. © 1993 Wiley-Liss, Inc.
    Additional Material: 9 Ill.
    Type of Medium: Electronic Resource
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