The vitronectin receptor alpha-V beta-3, contrary to ICAM-1, is not modulated by interferon-gamma and tumour necrosis factor-alpha on melanoma cell lines
A correlation was recently shown between expression of the vitronectin receptor (VnR) and the tumorigenic capacity of cultured human melanoma cell lines. On the other hand, modulation of VnR expression by interferon-gamma (IFN-gamma) and tumour necrosis factor-alpha (TNF-alpha) was observed on diffe...
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Veröffentlicht in: | Acta dermato-venereologica 1996-07, Vol.76 (4), p.269-273 |
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container_title | Acta dermato-venereologica |
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creator | BOCCALETTI, V TEMPONI, M WANG, Z MANGANONI, A. M MARCELLI, M MAIO, M FERRONE, S DE PANFILIS, G |
description | A correlation was recently shown between expression of the vitronectin receptor (VnR) and the tumorigenic capacity of cultured human melanoma cell lines. On the other hand, modulation of VnR expression by interferon-gamma (IFN-gamma) and tumour necrosis factor-alpha (TNF-alpha) was observed on different non-melanoma cell lines. We tested IFN-gamma, TNF-alpha and interleukin-2 (IL-2), which are presumably released by infiltrating leukocytes in the melanoma lesional environment, on three melanoma cell lines. The VnR expression was assessed using FACS analysis and radioimmunolabelling. The VnR did not show any modulation after treatment with any of the cytokines tested. By contrast, the expression of the intercellular adhesion molecule-1 (ICAM-1), tested as control, on five melanoma cell lines, was greatly enhanced by IFN-gamma and TNF-alpha. Thus, some host cytokines may preferentially induce melanoma cells to express ICAM-1 (which can increase host cytotoxic response against melanoma), other than the VnR (which instead might contribute to melanoma metastasis). |
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M ; MARCELLI, M ; MAIO, M ; FERRONE, S ; DE PANFILIS, G</creator><creatorcontrib>BOCCALETTI, V ; TEMPONI, M ; WANG, Z ; MANGANONI, A. M ; MARCELLI, M ; MAIO, M ; FERRONE, S ; DE PANFILIS, G</creatorcontrib><description>A correlation was recently shown between expression of the vitronectin receptor (VnR) and the tumorigenic capacity of cultured human melanoma cell lines. On the other hand, modulation of VnR expression by interferon-gamma (IFN-gamma) and tumour necrosis factor-alpha (TNF-alpha) was observed on different non-melanoma cell lines. We tested IFN-gamma, TNF-alpha and interleukin-2 (IL-2), which are presumably released by infiltrating leukocytes in the melanoma lesional environment, on three melanoma cell lines. The VnR expression was assessed using FACS analysis and radioimmunolabelling. The VnR did not show any modulation after treatment with any of the cytokines tested. By contrast, the expression of the intercellular adhesion molecule-1 (ICAM-1), tested as control, on five melanoma cell lines, was greatly enhanced by IFN-gamma and TNF-alpha. Thus, some host cytokines may preferentially induce melanoma cells to express ICAM-1 (which can increase host cytotoxic response against melanoma), other than the VnR (which instead might contribute to melanoma metastasis).</description><identifier>ISSN: 0001-5555</identifier><identifier>EISSN: 1651-2057</identifier><identifier>DOI: 10.2340/0001555576269273</identifier><identifier>PMID: 8869681</identifier><identifier>CODEN: ADVEA4</identifier><language>eng</language><publisher>Uppsala: Acta dermato-venereologica</publisher><subject>Biological and medical sciences ; Cytotoxicity, Immunologic - genetics ; Dermatology ; Fluorescent Antibody Technique, Indirect ; Gene Expression Regulation, Neoplastic ; Humans ; Intercellular Adhesion Molecule-1 - genetics ; Intercellular Adhesion Molecule-1 - immunology ; Interferon-gamma - pharmacology ; Interleukin-2 - pharmacology ; Medical sciences ; Melanoma - genetics ; Melanoma - metabolism ; Melanoma - secondary ; Radioimmunodetection ; Receptors, Vitronectin - genetics ; Receptors, Vitronectin - immunology ; Skin Neoplasms - genetics ; Skin Neoplasms - metabolism ; Tumor Cells, Cultured ; Tumor Necrosis Factor-alpha - pharmacology ; Tumors of the skin and soft tissue. Premalignant lesions</subject><ispartof>Acta dermato-venereologica, 1996-07, Vol.76 (4), p.269-273</ispartof><rights>1996 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c365t-57dad1bb3da6a18853ff4fb23aae504f4569acf9a7a78100bd3a3bdb0c04e7033</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27923,27924</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=3178685$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/8869681$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>BOCCALETTI, V</creatorcontrib><creatorcontrib>TEMPONI, M</creatorcontrib><creatorcontrib>WANG, Z</creatorcontrib><creatorcontrib>MANGANONI, A. M</creatorcontrib><creatorcontrib>MARCELLI, M</creatorcontrib><creatorcontrib>MAIO, M</creatorcontrib><creatorcontrib>FERRONE, S</creatorcontrib><creatorcontrib>DE PANFILIS, G</creatorcontrib><title>The vitronectin receptor alpha-V beta-3, contrary to ICAM-1, is not modulated by interferon-gamma and tumour necrosis factor-alpha on melanoma cell lines</title><title>Acta dermato-venereologica</title><addtitle>Acta Derm Venereol</addtitle><description>A correlation was recently shown between expression of the vitronectin receptor (VnR) and the tumorigenic capacity of cultured human melanoma cell lines. On the other hand, modulation of VnR expression by interferon-gamma (IFN-gamma) and tumour necrosis factor-alpha (TNF-alpha) was observed on different non-melanoma cell lines. We tested IFN-gamma, TNF-alpha and interleukin-2 (IL-2), which are presumably released by infiltrating leukocytes in the melanoma lesional environment, on three melanoma cell lines. The VnR expression was assessed using FACS analysis and radioimmunolabelling. The VnR did not show any modulation after treatment with any of the cytokines tested. By contrast, the expression of the intercellular adhesion molecule-1 (ICAM-1), tested as control, on five melanoma cell lines, was greatly enhanced by IFN-gamma and TNF-alpha. Thus, some host cytokines may preferentially induce melanoma cells to express ICAM-1 (which can increase host cytotoxic response against melanoma), other than the VnR (which instead might contribute to melanoma metastasis).</description><subject>Biological and medical sciences</subject><subject>Cytotoxicity, Immunologic - genetics</subject><subject>Dermatology</subject><subject>Fluorescent Antibody Technique, Indirect</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Humans</subject><subject>Intercellular Adhesion Molecule-1 - genetics</subject><subject>Intercellular Adhesion Molecule-1 - immunology</subject><subject>Interferon-gamma - pharmacology</subject><subject>Interleukin-2 - pharmacology</subject><subject>Medical sciences</subject><subject>Melanoma - genetics</subject><subject>Melanoma - metabolism</subject><subject>Melanoma - secondary</subject><subject>Radioimmunodetection</subject><subject>Receptors, Vitronectin - genetics</subject><subject>Receptors, Vitronectin - immunology</subject><subject>Skin Neoplasms - genetics</subject><subject>Skin Neoplasms - metabolism</subject><subject>Tumor Cells, Cultured</subject><subject>Tumor Necrosis Factor-alpha - pharmacology</subject><subject>Tumors of the skin and soft tissue. Premalignant lesions</subject><issn>0001-5555</issn><issn>1651-2057</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1996</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdUc1vFSEQJ8amPqt3LyYcjKdSYVlg39E0fiU1vVSvmwEGu2YXnsA26Z_S_1bWvvTgXMjk98XMEPJG8ItO9vwD51yoVkZ3et8Z-YzshFaCdVyZ52S3wWzDX5CXpfxubafEcEpOh0Hv9SB25OHmFundVHOK6OoUaUaHh5oyhflwC-wntViByXPqUqwZ8j2tiX67_PidiXM6FRpTpUvy6wwVPbX3dIoVc8BmyH7BsgCF6Gldl7Rm2jJyKk0VwLUM9i-DpkgXnCGmRnY4z3SeIpZX5CTAXPD18T0jPz5_urn8yq6uv7T8K-akVpUp48ELa6UHDWIYlAyhD7aTAKh4H3ql9-DCHgyYQXBuvQRpveWO92i4lGfk_aPvIac_K5Y6LlPZvgER01pGM_RKSSkakT8StxlKxjAe8rS0jYyCj9s1xv-v0SRvj96rXdA_CY7rb_i7Iw7FwRwyRDeVJ5oUZtBtor9D5ZNF</recordid><startdate>19960701</startdate><enddate>19960701</enddate><creator>BOCCALETTI, V</creator><creator>TEMPONI, M</creator><creator>WANG, Z</creator><creator>MANGANONI, A. M</creator><creator>MARCELLI, M</creator><creator>MAIO, M</creator><creator>FERRONE, S</creator><creator>DE PANFILIS, G</creator><general>Acta dermato-venereologica</general><scope>IQODW</scope><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>19960701</creationdate><title>The vitronectin receptor alpha-V beta-3, contrary to ICAM-1, is not modulated by interferon-gamma and tumour necrosis factor-alpha on melanoma cell lines</title><author>BOCCALETTI, V ; TEMPONI, M ; WANG, Z ; MANGANONI, A. M ; MARCELLI, M ; MAIO, M ; FERRONE, S ; DE PANFILIS, G</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c365t-57dad1bb3da6a18853ff4fb23aae504f4569acf9a7a78100bd3a3bdb0c04e7033</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1996</creationdate><topic>Biological and medical sciences</topic><topic>Cytotoxicity, Immunologic - genetics</topic><topic>Dermatology</topic><topic>Fluorescent Antibody Technique, Indirect</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Humans</topic><topic>Intercellular Adhesion Molecule-1 - genetics</topic><topic>Intercellular Adhesion Molecule-1 - immunology</topic><topic>Interferon-gamma - pharmacology</topic><topic>Interleukin-2 - pharmacology</topic><topic>Medical sciences</topic><topic>Melanoma - genetics</topic><topic>Melanoma - metabolism</topic><topic>Melanoma - secondary</topic><topic>Radioimmunodetection</topic><topic>Receptors, Vitronectin - genetics</topic><topic>Receptors, Vitronectin - immunology</topic><topic>Skin Neoplasms - genetics</topic><topic>Skin Neoplasms - metabolism</topic><topic>Tumor Cells, Cultured</topic><topic>Tumor Necrosis Factor-alpha - pharmacology</topic><topic>Tumors of the skin and soft tissue. Premalignant lesions</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>BOCCALETTI, V</creatorcontrib><creatorcontrib>TEMPONI, M</creatorcontrib><creatorcontrib>WANG, Z</creatorcontrib><creatorcontrib>MANGANONI, A. M</creatorcontrib><creatorcontrib>MARCELLI, M</creatorcontrib><creatorcontrib>MAIO, M</creatorcontrib><creatorcontrib>FERRONE, S</creatorcontrib><creatorcontrib>DE PANFILIS, G</creatorcontrib><collection>Pascal-Francis</collection><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>Acta dermato-venereologica</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>BOCCALETTI, V</au><au>TEMPONI, M</au><au>WANG, Z</au><au>MANGANONI, A. M</au><au>MARCELLI, M</au><au>MAIO, M</au><au>FERRONE, S</au><au>DE PANFILIS, G</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The vitronectin receptor alpha-V beta-3, contrary to ICAM-1, is not modulated by interferon-gamma and tumour necrosis factor-alpha on melanoma cell lines</atitle><jtitle>Acta dermato-venereologica</jtitle><addtitle>Acta Derm Venereol</addtitle><date>1996-07-01</date><risdate>1996</risdate><volume>76</volume><issue>4</issue><spage>269</spage><epage>273</epage><pages>269-273</pages><issn>0001-5555</issn><eissn>1651-2057</eissn><coden>ADVEA4</coden><abstract>A correlation was recently shown between expression of the vitronectin receptor (VnR) and the tumorigenic capacity of cultured human melanoma cell lines. On the other hand, modulation of VnR expression by interferon-gamma (IFN-gamma) and tumour necrosis factor-alpha (TNF-alpha) was observed on different non-melanoma cell lines. We tested IFN-gamma, TNF-alpha and interleukin-2 (IL-2), which are presumably released by infiltrating leukocytes in the melanoma lesional environment, on three melanoma cell lines. The VnR expression was assessed using FACS analysis and radioimmunolabelling. The VnR did not show any modulation after treatment with any of the cytokines tested. By contrast, the expression of the intercellular adhesion molecule-1 (ICAM-1), tested as control, on five melanoma cell lines, was greatly enhanced by IFN-gamma and TNF-alpha. Thus, some host cytokines may preferentially induce melanoma cells to express ICAM-1 (which can increase host cytotoxic response against melanoma), other than the VnR (which instead might contribute to melanoma metastasis).</abstract><cop>Uppsala</cop><pub>Acta dermato-venereologica</pub><pmid>8869681</pmid><doi>10.2340/0001555576269273</doi><tpages>5</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Biological and medical sciences Cytotoxicity, Immunologic - genetics Dermatology Fluorescent Antibody Technique, Indirect Gene Expression Regulation, Neoplastic Humans Intercellular Adhesion Molecule-1 - genetics Intercellular Adhesion Molecule-1 - immunology Interferon-gamma - pharmacology Interleukin-2 - pharmacology Medical sciences Melanoma - genetics Melanoma - metabolism Melanoma - secondary Radioimmunodetection Receptors, Vitronectin - genetics Receptors, Vitronectin - immunology Skin Neoplasms - genetics Skin Neoplasms - metabolism Tumor Cells, Cultured Tumor Necrosis Factor-alpha - pharmacology Tumors of the skin and soft tissue. Premalignant lesions |
title | The vitronectin receptor alpha-V beta-3, contrary to ICAM-1, is not modulated by interferon-gamma and tumour necrosis factor-alpha on melanoma cell lines |
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