Modulation of the growth of transformed cells by human tumor necrosis factor-alpha and interferon-gamma
Recombinant human tumor necrosis factor-alpha (rHuTNF-alpha) inhibited growth of the cervical carcinoma cell line, ME-180neo, at doses greater than 50 units/ml, but stimulated the growth of these cells at low doses (0.1-10 units/ml). ME-180neo variants selected for resistance to the cytotoxic effect...
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| Veröffentlicht in: | Cancer research (Chicago, Ill.) Ill.), 1987-10, Vol.47 (20), p.5382-5385 |
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| container_issue | 20 |
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| container_title | Cancer research (Chicago, Ill.) |
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| creator | Lewis, G D Aggarwal, B B Eessalu, T E Sugarman, B J Shepard, H M |
| description | Recombinant human tumor necrosis factor-alpha (rHuTNF-alpha) inhibited growth of the cervical carcinoma cell line, ME-180neo, at doses greater than 50 units/ml, but stimulated the growth of these cells at low doses (0.1-10 units/ml). ME-180neo variants selected for resistance to the cytotoxic effects of rHuTNF-alpha retained the ability to be growth stimulated at all concentrations tested. ME-180neo cells and the rHuTNF-alpha-resistant ME-180neo variants possessed equivalent steady state numbers of TNF-alpha receptors with similar Kd values. Recombinant human interferon-gamma (rHuIFN-gamma) augmented the rHuTNF-alpha-induced cytotoxic response of ME-180neo cells and overcame the resistance of the ME-180neo variants to rHuTNF-alpha cytotoxicity. In separate experiments we were able to show that the number of TNF-alpha binding sites on both rHuTNF-alpha-sensitive and -resistant ME-180neo cells was similar and was increased by treatment with rHuIFN-gamma. These results suggest that the growth stimulation of tumor cells mediated by rHuTNF-alpha can be dissociated from the cytotoxic response and that these responses are not related to the number or affinity of TNF-alpha binding sites. |
| format | Article |
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ME-180neo variants selected for resistance to the cytotoxic effects of rHuTNF-alpha retained the ability to be growth stimulated at all concentrations tested. ME-180neo cells and the rHuTNF-alpha-resistant ME-180neo variants possessed equivalent steady state numbers of TNF-alpha receptors with similar Kd values. Recombinant human interferon-gamma (rHuIFN-gamma) augmented the rHuTNF-alpha-induced cytotoxic response of ME-180neo cells and overcame the resistance of the ME-180neo variants to rHuTNF-alpha cytotoxicity. In separate experiments we were able to show that the number of TNF-alpha binding sites on both rHuTNF-alpha-sensitive and -resistant ME-180neo cells was similar and was increased by treatment with rHuIFN-gamma. These results suggest that the growth stimulation of tumor cells mediated by rHuTNF-alpha can be dissociated from the cytotoxic response and that these responses are not related to the number or affinity of TNF-alpha binding sites.</description><identifier>ISSN: 0008-5472</identifier><identifier>PMID: 2820567</identifier><language>eng</language><publisher>United States</publisher><subject>Cell Division - drug effects ; Cell Line ; Cell Transformation, Neoplastic - drug effects ; Female ; Humans ; Interferon-gamma - pharmacology ; Kinetics ; Receptors, Cell Surface - metabolism ; Receptors, Tumor Necrosis Factor ; Recombinant Proteins - pharmacology ; Tumor Necrosis Factor-alpha - pharmacology ; Uterine Cervical Neoplasms - pathology</subject><ispartof>Cancer research (Chicago, Ill.), 1987-10, Vol.47 (20), p.5382-5385</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>315,781,785</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/2820567$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lewis, G D</creatorcontrib><creatorcontrib>Aggarwal, B B</creatorcontrib><creatorcontrib>Eessalu, T E</creatorcontrib><creatorcontrib>Sugarman, B J</creatorcontrib><creatorcontrib>Shepard, H M</creatorcontrib><title>Modulation of the growth of transformed cells by human tumor necrosis factor-alpha and interferon-gamma</title><title>Cancer research (Chicago, Ill.)</title><addtitle>Cancer Res</addtitle><description>Recombinant human tumor necrosis factor-alpha (rHuTNF-alpha) inhibited growth of the cervical carcinoma cell line, ME-180neo, at doses greater than 50 units/ml, but stimulated the growth of these cells at low doses (0.1-10 units/ml). ME-180neo variants selected for resistance to the cytotoxic effects of rHuTNF-alpha retained the ability to be growth stimulated at all concentrations tested. ME-180neo cells and the rHuTNF-alpha-resistant ME-180neo variants possessed equivalent steady state numbers of TNF-alpha receptors with similar Kd values. Recombinant human interferon-gamma (rHuIFN-gamma) augmented the rHuTNF-alpha-induced cytotoxic response of ME-180neo cells and overcame the resistance of the ME-180neo variants to rHuTNF-alpha cytotoxicity. In separate experiments we were able to show that the number of TNF-alpha binding sites on both rHuTNF-alpha-sensitive and -resistant ME-180neo cells was similar and was increased by treatment with rHuIFN-gamma. These results suggest that the growth stimulation of tumor cells mediated by rHuTNF-alpha can be dissociated from the cytotoxic response and that these responses are not related to the number or affinity of TNF-alpha binding sites.</description><subject>Cell Division - drug effects</subject><subject>Cell Line</subject><subject>Cell Transformation, Neoplastic - drug effects</subject><subject>Female</subject><subject>Humans</subject><subject>Interferon-gamma - pharmacology</subject><subject>Kinetics</subject><subject>Receptors, Cell Surface - metabolism</subject><subject>Receptors, Tumor Necrosis Factor</subject><subject>Recombinant Proteins - pharmacology</subject><subject>Tumor Necrosis Factor-alpha - pharmacology</subject><subject>Uterine Cervical Neoplasms - pathology</subject><issn>0008-5472</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1987</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNotkE1LxDAYhHNQ1nX1Jwg5eSskaZM0R1n8ghUvei5p-qatNElNUmT_vdXd0zDwMMzMBdoSQuqCV5JdoeuUvlbLKeEbtGE1I1zILerfQrdMOo_B42BxHgD3Mfzk4d9F7ZMN0UGHDUxTwu0RD4vTHufFhYg9mBjSmLDVJodY6GkeNNa-w6PPEC3E4IteO6dv0KXVU4Lbs-7Q59Pjx_6lOLw_v-4fDsXMiMgF7wgYxipBFafGkoqrqmREqloISS2VijMFXFkLrOwMA0WlNKQVRnIppCx36P6UO8fwvUDKjRvTX3ftISypqel6SU3qFbw7g0u77mvmODodj835mfIXlX9eqA</recordid><startdate>19871015</startdate><enddate>19871015</enddate><creator>Lewis, G D</creator><creator>Aggarwal, B B</creator><creator>Eessalu, T E</creator><creator>Sugarman, B J</creator><creator>Shepard, H M</creator><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7X8</scope></search><sort><creationdate>19871015</creationdate><title>Modulation of the growth of transformed cells by human tumor necrosis factor-alpha and interferon-gamma</title><author>Lewis, G D ; Aggarwal, B B ; Eessalu, T E ; Sugarman, B J ; Shepard, H M</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-p206t-5d0ec22461951cf045943207986671f179529e59ffe23dc2e9177c0b6c7576773</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1987</creationdate><topic>Cell Division - drug effects</topic><topic>Cell Line</topic><topic>Cell Transformation, Neoplastic - drug effects</topic><topic>Female</topic><topic>Humans</topic><topic>Interferon-gamma - pharmacology</topic><topic>Kinetics</topic><topic>Receptors, Cell Surface - metabolism</topic><topic>Receptors, Tumor Necrosis Factor</topic><topic>Recombinant Proteins - pharmacology</topic><topic>Tumor Necrosis Factor-alpha - pharmacology</topic><topic>Uterine Cervical Neoplasms - pathology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lewis, G D</creatorcontrib><creatorcontrib>Aggarwal, B B</creatorcontrib><creatorcontrib>Eessalu, T E</creatorcontrib><creatorcontrib>Sugarman, B J</creatorcontrib><creatorcontrib>Shepard, H M</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>MEDLINE - Academic</collection><jtitle>Cancer research (Chicago, Ill.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lewis, G D</au><au>Aggarwal, B B</au><au>Eessalu, T E</au><au>Sugarman, B J</au><au>Shepard, H M</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Modulation of the growth of transformed cells by human tumor necrosis factor-alpha and interferon-gamma</atitle><jtitle>Cancer research (Chicago, Ill.)</jtitle><addtitle>Cancer Res</addtitle><date>1987-10-15</date><risdate>1987</risdate><volume>47</volume><issue>20</issue><spage>5382</spage><epage>5385</epage><pages>5382-5385</pages><issn>0008-5472</issn><abstract>Recombinant human tumor necrosis factor-alpha (rHuTNF-alpha) inhibited growth of the cervical carcinoma cell line, ME-180neo, at doses greater than 50 units/ml, but stimulated the growth of these cells at low doses (0.1-10 units/ml). ME-180neo variants selected for resistance to the cytotoxic effects of rHuTNF-alpha retained the ability to be growth stimulated at all concentrations tested. ME-180neo cells and the rHuTNF-alpha-resistant ME-180neo variants possessed equivalent steady state numbers of TNF-alpha receptors with similar Kd values. Recombinant human interferon-gamma (rHuIFN-gamma) augmented the rHuTNF-alpha-induced cytotoxic response of ME-180neo cells and overcame the resistance of the ME-180neo variants to rHuTNF-alpha cytotoxicity. In separate experiments we were able to show that the number of TNF-alpha binding sites on both rHuTNF-alpha-sensitive and -resistant ME-180neo cells was similar and was increased by treatment with rHuIFN-gamma. These results suggest that the growth stimulation of tumor cells mediated by rHuTNF-alpha can be dissociated from the cytotoxic response and that these responses are not related to the number or affinity of TNF-alpha binding sites.</abstract><cop>United States</cop><pmid>2820567</pmid><tpages>4</tpages></addata></record> |
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| ispartof | Cancer research (Chicago, Ill.), 1987-10, Vol.47 (20), p.5382-5385 |
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| language | eng |
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| source | MEDLINE; American Association for Cancer Research; EZB-FREE-00999 freely available EZB journals |
| subjects | Cell Division - drug effects Cell Line Cell Transformation, Neoplastic - drug effects Female Humans Interferon-gamma - pharmacology Kinetics Receptors, Cell Surface - metabolism Receptors, Tumor Necrosis Factor Recombinant Proteins - pharmacology Tumor Necrosis Factor-alpha - pharmacology Uterine Cervical Neoplasms - pathology |
| title | Modulation of the growth of transformed cells by human tumor necrosis factor-alpha and interferon-gamma |
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