Mechanism of tumor cell-induced T-cell apoptosis mediated by galectin-1
| Autor: | Éva Monostori, Robert L. Katona, Vilmos Tubak, Ferenc Uher, László Krenács, Andrea Blaskó, Gábor J. Szebeni, Roberta Fajka-Boja, Ferenc Kovács-Sólyom, Robert Kiss, Lea Végh, Julianna Novák |
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| Rok vydání: | 2010 |
| Předmět: |
Galectin 1
CD30 T-Lymphocytes Immunology Apoptosis Cell Communication Biology Jurkat cells HeLa Jurkat Cells Neoplasms Humans Immunology and Allergy Cytotoxic T cell Transgenes RNA Small Interfering Membrane Potential Mitochondrial ZAP-70 Protein-Tyrosine Kinase ZAP70 biology.organism_classification Coculture Techniques Mitochondria Neoplasm Proteins Cell biology Gene Expression Regulation Neoplastic Tumor Escape Lymphocyte Specific Protein Tyrosine Kinase p56(lck) Tumor progression Caspases Disease Progression Cancer research HeLa Cells |
| Zdroj: | Immunology Letters. 127:108-118 |
| ISSN: | 0165-2478 |
| Popis: | Galectin-1 (Gal-1) has been implicated in tumor progression partly via the induction of T-cell apoptosis. However the mechanism of Gal-1 induced T-cell death was mostly studied using recombinant, soluble Gal-1 producing controversial results. To explore the true mechanism of Gal-1 and hence tumor cell-induced T-cell death, we applied co-cultures of tumor cells and T-cells thus avoiding artificial circumstances generated using recombinant protein. T-cells died when co-cultured with Gal-1-expressing but survived with Gal-1 non-expressing tumor cells. Removing tumor cell surface Gal-1 or knocking down Gal-1 expression resulted in diminution of T-cell apoptosis. Gal-1 transgenic or soluble Gal-1 treated HeLa cells became cytotoxic. Stimulation of apoptosis required interaction between the tumor and T-cells, presence of p56lck and ZAP70, decrease of mitochondrial membrane potential and caspase activation. Hence tumor cell-derived Gal-1 might efficiently contribute to tumor self-defense. Moreover this system resolves the discrepancies obtained using recombinant Gal-1 in T-cell apoptosis studies. |
| Databáze: | OpenAIRE |
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