Glycoprotein 170 Induces Platelet-Activating Factor Receptor Membrane Expression and Confers Tumor Cell Hypersensitivity to NK-Dependent Cell Lysis
Autor: | Christina Fleet, Yves Denizot, Jean-François Bourge, Philippe Leboulch, Rob Pawliuk, François Sigaux, Christian Berthou, Eugene Michel, Daniela Geromin, Annie Soulié, Marilyne Sasportes |
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Přispěvatelé: | Physiologie Moléculaire de la Réponse Immune et des Lymphoproliférations (PMRIL), Université de Limoges (UNILIM)-Génomique, Environnement, Immunité, Santé, Thérapeutique (GEIST FR CNRS 3503)-Centre National de la Recherche Scientifique (CNRS), Carrion, Claire |
Rok vydání: | 2004 |
Předmět: |
Cytotoxicity
Immunologic MESH: Hydrogen-Ion Concentration Lysis Cell MESH: Receptors G-Protein-Coupled Receptors G-Protein-Coupled Interleukin 21 Transduction Genetic Immunology and Allergy Teratoma MESH: Teratoma Hydrogen-Ion Concentration MESH: Transduction Genetic MESH: Drug Resistance Neoplasm Cell biology Killer Cells Natural MESH: Retroviridae medicine.anatomical_structure Cell killing Interleukin 12 [SDV.IMM]Life Sciences [q-bio]/Immunology MESH: Leukemia Erythroblastic Acute MESH: Killer Cells Natural ATP Binding Cassette Transporter Subfamily B NLM MESH: Cell Line Tumor [SDV.IMM] Life Sciences [q-bio]/Immunology Paclitaxel Immunology MESH: Glycoproteins MESH: Carcinoma Embryonal Platelet Membrane Glycoproteins Biology Transfection Carcinoma Embryonal Cell Line Tumor medicine Humans MESH: Paclitaxel MESH: Cytotoxicity Immunologic Platelet Activating Factor Glycoproteins MESH: K562 Cells MESH: Platelet Activating Factor MESH: Humans Lymphokine-activated killer cell MESH: Transfection Cell Membrane MESH: Clone Cells MESH: Platelet Membrane Glycoproteins Molecular biology Clone Cells Retroviridae Perforin Drug Resistance Neoplasm biology.protein Leukemia Erythroblastic Acute MESH: Genes MDR Genes MDR K562 Cells MESH: Cell Membrane K562 cells |
Zdroj: | Journal of Immunology Journal of Immunology, Publisher : Baltimore : Williams & Wilkins, c1950-. Latest Publisher : Bethesda, MD : American Association of Immunologists, 2004, 172 (6), pp.3604-11 |
ISSN: | 1550-6606 0022-1767 |
Popis: | Multidrug resistance (MDR) confers resistance to anticancer drugs and reduces therapeutic efficiency. It is often characterized by the expression of the MDR1 gene product P-glycoprotein (or gp170) at the membrane of tumor cells. To further propose a potential complementary tool in cancer treatment, the sensitivity of gp170 tumor cells to NK-dependent lysis was investigated. Two kinds of cells were generated from wild-type K562 erythroleukemic cells: the first were derived from Taxol-selected cells and cloned, whereas the second were retrovirally transduced by the cDNA of the MDR1 gene. The last process was also applied to the human embryonal carcinoma cells called Tera-2 cells. First, both cloned and MDR-1 K562 cells appeared highly susceptible to naive NK cell killing. Interestingly, in addition, Tera-2 cells that were not sensitive to NK lysis could be killed when they expressed gp170 at their membranes. In previous data, we demonstrated that NK cell release of bimolecular complexes composed of perforin and platelet-activating factor (PAF) interacting with the PAF-R, which has to be expressed on the target cell membranes, were components of NK tumor cell killing. In the present study, we show that gp170 has the capacity to drive constitutive PAF-R expression on tumor cells, which could be responsible for hypersensitivity to NK lysis and accelerated cell death. |
Databáze: | OpenAIRE |
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