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Title: Tumor suppressor KAI1 affects integrin {alpha}v{beta}3-mediated ovarian cancer cell adhesion, motility, and proliferation

Abstract

The tetraspanin KAI1 had been described as a metastasis suppressor in many different cancer types, a function for which associations of KAI1 with adhesion and signaling receptors of the integrin superfamily likely play a role. In ovarian cancer, integrin {alpha}v{beta}3 correlates with tumor progression and its elevation in vitro provoked enhanced cell adhesion accompanied by significant increases in cell motility and proliferation in the presence of its major ligand vitronectin. In the present study, we characterized integrin {alpha}v{beta}3-mediated tumor biological effects as a function of cellular KAI1 restoration and proved for the first time that KAI1, besides its already known physical crosstalk with {beta}1-integrins, also colocalizes with integrin {alpha}v{beta}3. Functionally, elevated KAI1 levels drastically increased integrin {alpha}v{beta}3/vitronectin-dependent ovarian cancer cell adhesion. Since an intermediate level of cell adhesive strength is required for optimal cell migration, we next studied ovarian cancer cell motility as a function of KAI1 restoration. By time lapse video microscopy, we found impaired integrin {alpha}v{beta}3/vitronectin-mediated cell migration most probably due to strongly enhanced cellular immobilization onto the adhesion-supporting matrix. Moreover, KAI1 reexpression significantly diminished cell proliferation. These data strongly indicate that KAI1 may suppress ovarian cancer progression by inhibiting integrin {alpha}v{beta}3/vitronectin-provoked tumor cell motility and proliferation asmore » important hallmarks of the oncogenic process.« less

Authors:
;  [1];  [2];  [3];  [2];  [1];  [4];  [1]
  1. Clinical Research Unit, Department of Gynecology and Obstetrics, Technische Universitaet Muenchen Ismaninger Str. 22, D-81675 Munich (Germany)
  2. Institute of Pathology, Technische Universitaet Muenchen (Germany)
  3. Institute of Pathology, Technische Universitaet Dresden (Germany)
  4. Gynecol. Tumor Genetics, Department of Gynecology and Obstetrics, Technische Universitaet Muenchen (Germany)
Publication Date:
OSTI Identifier:
22209772
Resource Type:
Journal Article
Journal Name:
Experimental Cell Research
Additional Journal Information:
Journal Volume: 315; Journal Issue: 10; Other Information: Copyright (c) 2009 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved.; Country of input: International Atomic Energy Agency (IAEA); Journal ID: ISSN 0014-4827
Country of Publication:
United States
Language:
English
Subject:
60 APPLIED LIFE SCIENCES; BIOLOGICAL EFFECTS; CELL PROLIFERATION; IN VITRO; METASTASES; MICROSCOPY; NEOPLASMS; RECEPTORS; TUMOR CELLS

Citation Formats

Ruseva, Zlatna, Geiger, Pamina Xenia Charlotte, Hutzler, Peter, Kotzsch, Matthias, Luber, Birgit, Schmitt, Manfred, Gross, Eva, and Reuning, Ute. Tumor suppressor KAI1 affects integrin {alpha}v{beta}3-mediated ovarian cancer cell adhesion, motility, and proliferation. United States: N. p., 2009. Web. doi:10.1016/J.YEXCR.2009.01.007.
Ruseva, Zlatna, Geiger, Pamina Xenia Charlotte, Hutzler, Peter, Kotzsch, Matthias, Luber, Birgit, Schmitt, Manfred, Gross, Eva, & Reuning, Ute. Tumor suppressor KAI1 affects integrin {alpha}v{beta}3-mediated ovarian cancer cell adhesion, motility, and proliferation. United States. doi:10.1016/J.YEXCR.2009.01.007.
Ruseva, Zlatna, Geiger, Pamina Xenia Charlotte, Hutzler, Peter, Kotzsch, Matthias, Luber, Birgit, Schmitt, Manfred, Gross, Eva, and Reuning, Ute. Wed . "Tumor suppressor KAI1 affects integrin {alpha}v{beta}3-mediated ovarian cancer cell adhesion, motility, and proliferation". United States. doi:10.1016/J.YEXCR.2009.01.007.
@article{osti_22209772,
title = {Tumor suppressor KAI1 affects integrin {alpha}v{beta}3-mediated ovarian cancer cell adhesion, motility, and proliferation},
author = {Ruseva, Zlatna and Geiger, Pamina Xenia Charlotte and Hutzler, Peter and Kotzsch, Matthias and Luber, Birgit and Schmitt, Manfred and Gross, Eva and Reuning, Ute},
abstractNote = {The tetraspanin KAI1 had been described as a metastasis suppressor in many different cancer types, a function for which associations of KAI1 with adhesion and signaling receptors of the integrin superfamily likely play a role. In ovarian cancer, integrin {alpha}v{beta}3 correlates with tumor progression and its elevation in vitro provoked enhanced cell adhesion accompanied by significant increases in cell motility and proliferation in the presence of its major ligand vitronectin. In the present study, we characterized integrin {alpha}v{beta}3-mediated tumor biological effects as a function of cellular KAI1 restoration and proved for the first time that KAI1, besides its already known physical crosstalk with {beta}1-integrins, also colocalizes with integrin {alpha}v{beta}3. Functionally, elevated KAI1 levels drastically increased integrin {alpha}v{beta}3/vitronectin-dependent ovarian cancer cell adhesion. Since an intermediate level of cell adhesive strength is required for optimal cell migration, we next studied ovarian cancer cell motility as a function of KAI1 restoration. By time lapse video microscopy, we found impaired integrin {alpha}v{beta}3/vitronectin-mediated cell migration most probably due to strongly enhanced cellular immobilization onto the adhesion-supporting matrix. Moreover, KAI1 reexpression significantly diminished cell proliferation. These data strongly indicate that KAI1 may suppress ovarian cancer progression by inhibiting integrin {alpha}v{beta}3/vitronectin-provoked tumor cell motility and proliferation as important hallmarks of the oncogenic process.},
doi = {10.1016/J.YEXCR.2009.01.007},
journal = {Experimental Cell Research},
issn = {0014-4827},
number = 10,
volume = 315,
place = {United States},
year = {2009},
month = {6}
}