Mechanism of tumor cell-induced T-cell apoptosis mediated by galectin-1
Abstract 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...
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| Veröffentlicht in: | Immunology letters 2010-01, Vol.127 (2), p.108-118 |
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| creator | Kovács-Sólyom, Ferenc Blaskó, Andrea Fajka-Boja, Roberta Katona, Róbert L Végh, Lea Novák, Julianna Szebeni, Gábor János Krenács, László Uher, Ferenc Tubak, Vilmos Kiss, Robert Monostori, Éva |
| description | Abstract 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. |
| doi_str_mv | 10.1016/j.imlet.2009.10.003 |
| format | Article |
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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.</description><identifier>ISSN: 0165-2478</identifier><identifier>EISSN: 1879-0542</identifier><identifier>DOI: 10.1016/j.imlet.2009.10.003</identifier><identifier>PMID: 19874850</identifier><language>eng</language><publisher>Netherlands: Elsevier B.V</publisher><subject>Allergy and Immunology ; Apoptosis - immunology ; Caspases - metabolism ; Cell Communication ; Coculture Techniques ; Disease Progression ; Galectin 1 - genetics ; Galectin 1 - immunology ; Galectin 1 - metabolism ; Galectin-1 ; Gene Expression Regulation, Neoplastic ; HeLa Cells ; Humans ; Jurkat Cells ; Lymphocyte Specific Protein Tyrosine Kinase p56(lck) - genetics ; Lymphocyte Specific Protein Tyrosine Kinase p56(lck) - metabolism ; Membrane Potential, Mitochondrial ; Mitochondria - physiology ; Neoplasm Proteins - genetics ; Neoplasm Proteins - immunology ; Neoplasm Proteins - metabolism ; Neoplasms - immunology ; Neoplasms - pathology ; Neoplasms - physiopathology ; RNA, Small Interfering - genetics ; T-cell apoptosis ; T-Lymphocytes - immunology ; T-Lymphocytes - pathology ; Transgenes - genetics ; Tumor cells ; Tumor Escape ; Tumor-associated stroma cells ; ZAP-70 Protein-Tyrosine Kinase - genetics ; ZAP-70 Protein-Tyrosine Kinase - metabolism</subject><ispartof>Immunology letters, 2010-01, Vol.127 (2), p.108-118</ispartof><rights>Elsevier B.V.</rights><rights>2009 Elsevier B.V.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c413t-6bb2b51dfbac2de53f303da9f29dad58f7bbb7af0f92aa691da05e65803d192c3</citedby><cites>FETCH-LOGICAL-c413t-6bb2b51dfbac2de53f303da9f29dad58f7bbb7af0f92aa691da05e65803d192c3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0165247809002478$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27903,27904,65309</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19874850$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kovács-Sólyom, Ferenc</creatorcontrib><creatorcontrib>Blaskó, Andrea</creatorcontrib><creatorcontrib>Fajka-Boja, Roberta</creatorcontrib><creatorcontrib>Katona, Róbert L</creatorcontrib><creatorcontrib>Végh, Lea</creatorcontrib><creatorcontrib>Novák, Julianna</creatorcontrib><creatorcontrib>Szebeni, Gábor János</creatorcontrib><creatorcontrib>Krenács, László</creatorcontrib><creatorcontrib>Uher, Ferenc</creatorcontrib><creatorcontrib>Tubak, Vilmos</creatorcontrib><creatorcontrib>Kiss, Robert</creatorcontrib><creatorcontrib>Monostori, Éva</creatorcontrib><title>Mechanism of tumor cell-induced T-cell apoptosis mediated by galectin-1</title><title>Immunology letters</title><addtitle>Immunol Lett</addtitle><description>Abstract 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.</description><subject>Allergy and Immunology</subject><subject>Apoptosis - immunology</subject><subject>Caspases - metabolism</subject><subject>Cell Communication</subject><subject>Coculture Techniques</subject><subject>Disease Progression</subject><subject>Galectin 1 - genetics</subject><subject>Galectin 1 - immunology</subject><subject>Galectin 1 - metabolism</subject><subject>Galectin-1</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>HeLa Cells</subject><subject>Humans</subject><subject>Jurkat Cells</subject><subject>Lymphocyte Specific Protein Tyrosine Kinase p56(lck) - genetics</subject><subject>Lymphocyte Specific Protein Tyrosine Kinase p56(lck) - metabolism</subject><subject>Membrane Potential, Mitochondrial</subject><subject>Mitochondria - physiology</subject><subject>Neoplasm Proteins - genetics</subject><subject>Neoplasm Proteins - immunology</subject><subject>Neoplasm Proteins - metabolism</subject><subject>Neoplasms - immunology</subject><subject>Neoplasms - pathology</subject><subject>Neoplasms - physiopathology</subject><subject>RNA, Small Interfering - genetics</subject><subject>T-cell apoptosis</subject><subject>T-Lymphocytes - immunology</subject><subject>T-Lymphocytes - pathology</subject><subject>Transgenes - genetics</subject><subject>Tumor cells</subject><subject>Tumor Escape</subject><subject>Tumor-associated stroma cells</subject><subject>ZAP-70 Protein-Tyrosine Kinase - genetics</subject><subject>ZAP-70 Protein-Tyrosine Kinase - metabolism</subject><issn>0165-2478</issn><issn>1879-0542</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkU1v1DAQQC1ERZeWX4BU5cYpy9iOk_gAEqqgIBX10PZs-WMM3ibxYidI--_rsCshceE08vjN2POGkLcUthRo-363DeOA85YByJLZAvAXZEP7TtYgGvaSbAolatZ0_Tl5nfMOgAre8FfknMq-a3oBG3LzHe1PPYU8VtFX8zLGVFkchjpMbrHoqod6PVZ6H_dzzCFXI7qg53JjDtUPPaCdw1TTS3Lm9ZDxzSlekMcvnx-uv9a3dzffrj_d1rahfK5bY5gR1HmjLXMouOfAnZaeSaed6H1njOm0By-Z1q2kToPAVvSFopJZfkHeHfvuU_y1YJ7VGPL6Qz1hXLLqOGei4W1fSH4kbYo5J_Rqn8Ko00FRUKtAtVN_BKpV4JosAkvV1an_Ysqkf2tOxgrw4QhgmfJ3wKSyDTgVVSEVF8rF8J8HPv5Tb4cwBauHJzxg3sUlTUWgoiozBep-3eG6QpAAa-TPGumXzA</recordid><startdate>20100104</startdate><enddate>20100104</enddate><creator>Kovács-Sólyom, Ferenc</creator><creator>Blaskó, Andrea</creator><creator>Fajka-Boja, Roberta</creator><creator>Katona, Róbert L</creator><creator>Végh, Lea</creator><creator>Novák, Julianna</creator><creator>Szebeni, Gábor János</creator><creator>Krenács, László</creator><creator>Uher, Ferenc</creator><creator>Tubak, Vilmos</creator><creator>Kiss, Robert</creator><creator>Monostori, Éva</creator><general>Elsevier B.V</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>20100104</creationdate><title>Mechanism of tumor cell-induced T-cell apoptosis mediated by galectin-1</title><author>Kovács-Sólyom, Ferenc ; Blaskó, Andrea ; Fajka-Boja, Roberta ; Katona, Róbert L ; Végh, Lea ; Novák, Julianna ; Szebeni, Gábor János ; Krenács, László ; Uher, Ferenc ; Tubak, Vilmos ; Kiss, Robert ; Monostori, Éva</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c413t-6bb2b51dfbac2de53f303da9f29dad58f7bbb7af0f92aa691da05e65803d192c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2010</creationdate><topic>Allergy and Immunology</topic><topic>Apoptosis - immunology</topic><topic>Caspases - metabolism</topic><topic>Cell Communication</topic><topic>Coculture Techniques</topic><topic>Disease Progression</topic><topic>Galectin 1 - genetics</topic><topic>Galectin 1 - immunology</topic><topic>Galectin 1 - metabolism</topic><topic>Galectin-1</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>HeLa Cells</topic><topic>Humans</topic><topic>Jurkat Cells</topic><topic>Lymphocyte Specific Protein Tyrosine Kinase p56(lck) - genetics</topic><topic>Lymphocyte Specific Protein Tyrosine Kinase p56(lck) - metabolism</topic><topic>Membrane Potential, Mitochondrial</topic><topic>Mitochondria - physiology</topic><topic>Neoplasm Proteins - genetics</topic><topic>Neoplasm Proteins - immunology</topic><topic>Neoplasm Proteins - metabolism</topic><topic>Neoplasms - immunology</topic><topic>Neoplasms - pathology</topic><topic>Neoplasms - physiopathology</topic><topic>RNA, Small Interfering - genetics</topic><topic>T-cell apoptosis</topic><topic>T-Lymphocytes - immunology</topic><topic>T-Lymphocytes - pathology</topic><topic>Transgenes - genetics</topic><topic>Tumor cells</topic><topic>Tumor Escape</topic><topic>Tumor-associated stroma cells</topic><topic>ZAP-70 Protein-Tyrosine Kinase - genetics</topic><topic>ZAP-70 Protein-Tyrosine Kinase - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kovács-Sólyom, Ferenc</creatorcontrib><creatorcontrib>Blaskó, Andrea</creatorcontrib><creatorcontrib>Fajka-Boja, Roberta</creatorcontrib><creatorcontrib>Katona, Róbert L</creatorcontrib><creatorcontrib>Végh, Lea</creatorcontrib><creatorcontrib>Novák, Julianna</creatorcontrib><creatorcontrib>Szebeni, Gábor János</creatorcontrib><creatorcontrib>Krenács, László</creatorcontrib><creatorcontrib>Uher, Ferenc</creatorcontrib><creatorcontrib>Tubak, Vilmos</creatorcontrib><creatorcontrib>Kiss, Robert</creatorcontrib><creatorcontrib>Monostori, Éva</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Immunology letters</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kovács-Sólyom, Ferenc</au><au>Blaskó, Andrea</au><au>Fajka-Boja, Roberta</au><au>Katona, Róbert L</au><au>Végh, Lea</au><au>Novák, Julianna</au><au>Szebeni, Gábor János</au><au>Krenács, László</au><au>Uher, Ferenc</au><au>Tubak, Vilmos</au><au>Kiss, Robert</au><au>Monostori, Éva</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Mechanism of tumor cell-induced T-cell apoptosis mediated by galectin-1</atitle><jtitle>Immunology letters</jtitle><addtitle>Immunol Lett</addtitle><date>2010-01-04</date><risdate>2010</risdate><volume>127</volume><issue>2</issue><spage>108</spage><epage>118</epage><pages>108-118</pages><issn>0165-2478</issn><eissn>1879-0542</eissn><abstract>Abstract 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.</abstract><cop>Netherlands</cop><pub>Elsevier B.V</pub><pmid>19874850</pmid><doi>10.1016/j.imlet.2009.10.003</doi><tpages>11</tpages></addata></record> |
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| subjects | Allergy and Immunology Apoptosis - immunology Caspases - metabolism Cell Communication Coculture Techniques Disease Progression Galectin 1 - genetics Galectin 1 - immunology Galectin 1 - metabolism Galectin-1 Gene Expression Regulation, Neoplastic HeLa Cells Humans Jurkat Cells Lymphocyte Specific Protein Tyrosine Kinase p56(lck) - genetics Lymphocyte Specific Protein Tyrosine Kinase p56(lck) - metabolism Membrane Potential, Mitochondrial Mitochondria - physiology Neoplasm Proteins - genetics Neoplasm Proteins - immunology Neoplasm Proteins - metabolism Neoplasms - immunology Neoplasms - pathology Neoplasms - physiopathology RNA, Small Interfering - genetics T-cell apoptosis T-Lymphocytes - immunology T-Lymphocytes - pathology Transgenes - genetics Tumor cells Tumor Escape Tumor-associated stroma cells ZAP-70 Protein-Tyrosine Kinase - genetics ZAP-70 Protein-Tyrosine Kinase - metabolism |
| title | Mechanism of tumor cell-induced T-cell apoptosis mediated by galectin-1 |
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