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Interaction between elastin and tumor cell lines with different metastatic potential; in vitro and in vivo studies (1991)

Timar, J. ; Lapis, K. ; Fulop, T. ; [et al.]

Springer

Journal of cancer research and clinical oncology 117 (1991), S. 232-238

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ISSN: 1432-1335

Keywords: Elastin binding ; Elastin receptor ; Chemotaxis ; Ca2+ flux ; Lewis lung cell lines ; Cancer metastasis

Source: Springer Online Journal Archives 1860-2000

Topics: Medicine

Notes: Summary Interactions between the extracellular matrix macromolecules and tumor cells are critical in the process of metastasis formation. We show here that elastins (both mature insoluble elastin and a 75-kDa soluble peptide: κ-elastin) adhere rapidly to two cell lines with high metastatic capacities: a metastatic lung carcinoma cell line (3LL-HM) and a human amelanotic melanoma cell line (A-2058); by contrast the low-metastatic Lewis lung carcinoma cell line variant as well as a rhabdomyosarcoma cell line with a low metastatic potential bind to elastins to a much lower extent.3H-labelled κ-elastin was used in order to study elastin-3LL-HM interaction. It was found to be saturable (2 ng3H-labelled κ-elastin/106 cells), with one class of high-affinity binding sites having Kd equal to 1.3 nM and 16000 sites/cell. The binding of κ-elastin to 3LL-HM cells at its receptor triggered several cell responses; (a) increase of intracellular Ca2+ concentration; (b) induction of 3LL-HM chemotaxis toward the κ-elastin gradient; (c) stimulation of the adherence of mature insoluble elastin. In contrast to non-transformed cells such as fibroblasts and smooth muscle cells, the adhesion kinetics of insoluble elastin to 3LL-HM did not exhibit a lag period; the rapid binding of insoluble elastin to the tumor cells was followed by its slow detachment from the cells, which lasted for 6 h. 3LL-HM cells but not human skin fibroblasts were shown to secrete elastinolytic activity inhibitable by metal-chelating agents. In vivo studies were performed in order to evaluate the influence of κ-elastin binding to 3LL-HM cells on their ability to form lung colonies in mice. It was shown that pretreatment of 104 3LL-HM cells with 10 ΜM kelastin and the simultaneous i.v. injection into mice of 750 Μg κ-elastin together with the highly metastatic cells was able to reduce the number of lung colonies by more than 70% after 12 days.

Type of Medium: Electronic Resource

URL: http://dx.doi.org/10.1007/BF01625430

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PKC mediates 12(S)-HETE-induced cytoskeletal rearrangement in B16A melanoma cells (1993)

Timar, J. ; Tang, D. ; Bazaz, R. ; [et al.]

New York, NY : Wiley-Blackwell

Cell Motility and the Cytoskeleton 26 (1993), S. 49-65

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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.