STAT3 activation abrogates growth factor dependence and contributes to head and neck squamous cell carcinoma tumor growth in vivo
Epidermal growth factor receptor (EGFR) is up-regulated and contributes to the loss of growth control in squamous cell carcinoma of the head and neck (SCCHN). Previously, we reported an association between autocrine stimulation of EGFR and constitutive signal transducers and activators of transcript...
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| Veröffentlicht in: | Cell growth & differentiation 2002-08, Vol.13 (8), p.355-362 |
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| creator | KIJIMA, Taro NIWA, Hideo STEINMAN, Richard A DRENNING, Stephanie D GOODING, William E WENTZEL, Abbey L SICHUAN XI GRANDIS, Jennifer Rubin |
| description | Epidermal growth factor receptor (EGFR) is up-regulated and contributes to the loss of growth control in squamous cell carcinoma of the head and neck (SCCHN). Previously, we reported an association between autocrine stimulation of EGFR and constitutive signal transducers and activators of transcription (STAT) 3 activation in SCCHN cells in vitro and in vivo. Here, we evaluated the role of activated STAT3 in tumor progression and EGFR-independent mitogenic signaling. We found that SCCHN cells stably transfected with a dominant active STAT3 construct expressed elevated levels of STAT3 target genes, including Bcl-X(L) and cyclin D1, and demonstrated increased proliferation in vitro and more rapid tumor growth rates in vivo. Cell cycle analysis demonstrated an increased proportion of STAT3 construct transfectants in G(2)-M. These findings provide evidence that constitutive STAT3 activation contributes to tumor growth in SCCHN, independent of the EGFR autocrine axis. |
| format | Article |
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Previously, we reported an association between autocrine stimulation of EGFR and constitutive signal transducers and activators of transcription (STAT) 3 activation in SCCHN cells in vitro and in vivo. Here, we evaluated the role of activated STAT3 in tumor progression and EGFR-independent mitogenic signaling. We found that SCCHN cells stably transfected with a dominant active STAT3 construct expressed elevated levels of STAT3 target genes, including Bcl-X(L) and cyclin D1, and demonstrated increased proliferation in vitro and more rapid tumor growth rates in vivo. Cell cycle analysis demonstrated an increased proportion of STAT3 construct transfectants in G(2)-M. These findings provide evidence that constitutive STAT3 activation contributes to tumor growth in SCCHN, independent of the EGFR autocrine axis.</description><identifier>ISSN: 1044-9523</identifier><identifier>PMID: 12193474</identifier><language>eng</language><publisher>Philadelphia, PA: American Association for Cancer Research</publisher><subject>Autocrine Communication - genetics ; bcl-X Protein ; Biological and medical sciences ; Carcinoma, Squamous Cell - metabolism ; Carcinoma, Squamous Cell - physiopathology ; Cell Cycle - genetics ; Cell Division - genetics ; Cell physiology ; Cyclin D1 - genetics ; Cyclin D1 - metabolism ; DNA-Binding Proteins - genetics ; DNA-Binding Proteins - metabolism ; Epidermal Growth Factor - metabolism ; Fundamental and applied biological sciences. Psychology ; Gene Expression Regulation, Neoplastic - genetics ; Head and Neck Neoplasms - metabolism ; Head and Neck Neoplasms - physiopathology ; Humans ; Molecular and cellular biology ; Proto-Oncogene Proteins c-bcl-2 - genetics ; Proto-Oncogene Proteins c-bcl-2 - metabolism ; Receptor, Epidermal Growth Factor - genetics ; Signal transduction ; STAT3 Transcription Factor ; Trans-Activators - genetics ; Trans-Activators - metabolism ; Tumor Cells, Cultured</subject><ispartof>Cell growth & differentiation, 2002-08, Vol.13 (8), p.355-362</ispartof><rights>2002 INIST-CNRS</rights><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=13877902$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12193474$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>KIJIMA, Taro</creatorcontrib><creatorcontrib>NIWA, Hideo</creatorcontrib><creatorcontrib>STEINMAN, Richard A</creatorcontrib><creatorcontrib>DRENNING, Stephanie D</creatorcontrib><creatorcontrib>GOODING, William E</creatorcontrib><creatorcontrib>WENTZEL, Abbey L</creatorcontrib><creatorcontrib>SICHUAN XI</creatorcontrib><creatorcontrib>GRANDIS, Jennifer Rubin</creatorcontrib><title>STAT3 activation abrogates growth factor dependence and contributes to head and neck squamous cell carcinoma tumor growth in vivo</title><title>Cell growth & differentiation</title><addtitle>Cell Growth Differ</addtitle><description>Epidermal growth factor receptor (EGFR) is up-regulated and contributes to the loss of growth control in squamous cell carcinoma of the head and neck (SCCHN). Previously, we reported an association between autocrine stimulation of EGFR and constitutive signal transducers and activators of transcription (STAT) 3 activation in SCCHN cells in vitro and in vivo. Here, we evaluated the role of activated STAT3 in tumor progression and EGFR-independent mitogenic signaling. We found that SCCHN cells stably transfected with a dominant active STAT3 construct expressed elevated levels of STAT3 target genes, including Bcl-X(L) and cyclin D1, and demonstrated increased proliferation in vitro and more rapid tumor growth rates in vivo. Cell cycle analysis demonstrated an increased proportion of STAT3 construct transfectants in G(2)-M. These findings provide evidence that constitutive STAT3 activation contributes to tumor growth in SCCHN, independent of the EGFR autocrine axis.</description><subject>Autocrine Communication - genetics</subject><subject>bcl-X Protein</subject><subject>Biological and medical sciences</subject><subject>Carcinoma, Squamous Cell - metabolism</subject><subject>Carcinoma, Squamous Cell - physiopathology</subject><subject>Cell Cycle - genetics</subject><subject>Cell Division - genetics</subject><subject>Cell physiology</subject><subject>Cyclin D1 - genetics</subject><subject>Cyclin D1 - metabolism</subject><subject>DNA-Binding Proteins - genetics</subject><subject>DNA-Binding Proteins - metabolism</subject><subject>Epidermal Growth Factor - metabolism</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Gene Expression Regulation, Neoplastic - genetics</subject><subject>Head and Neck Neoplasms - metabolism</subject><subject>Head and Neck Neoplasms - physiopathology</subject><subject>Humans</subject><subject>Molecular and cellular biology</subject><subject>Proto-Oncogene Proteins c-bcl-2 - genetics</subject><subject>Proto-Oncogene Proteins c-bcl-2 - metabolism</subject><subject>Receptor, Epidermal Growth Factor - genetics</subject><subject>Signal transduction</subject><subject>STAT3 Transcription Factor</subject><subject>Trans-Activators - genetics</subject><subject>Trans-Activators - metabolism</subject><subject>Tumor Cells, Cultured</subject><issn>1044-9523</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2002</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpFkMtOwzAQRbMA0fL4BeQN7CrZsfNaVhUvqRILyjoa25PWkNip7RSx5M9JIYjVSPceHV3NSTJnVIhFlaV8lpyH8EYpE4zys2TGUlZxUYh58vWyWW44ARXNAaJxloD0bgsRA9l69xF3pBlL54nGHq1Gq5CA1UQ5G72RwxGMjuwQ9E9uUb2TsB-gc0MgCtuWKPDKWNcBiUM3miavseRgDu4yOW2gDXg13Yvk9f5us3pcrJ8fnlbL9aJPeREXjW6EViUgMiqrnOYylwVD1midKVYqxkQmZVNSkVGtUHGaF7qBCjM6Vlzzi-T219t7tx8wxLoz4bgPLI5T6yKlaVFxOoLXEzjIDnXde9OB_6z_njYCNxMAQUHbeLDKhH-Ol0VR0ZR_A2xxd2A</recordid><startdate>20020801</startdate><enddate>20020801</enddate><creator>KIJIMA, Taro</creator><creator>NIWA, Hideo</creator><creator>STEINMAN, Richard A</creator><creator>DRENNING, Stephanie D</creator><creator>GOODING, William E</creator><creator>WENTZEL, Abbey L</creator><creator>SICHUAN XI</creator><creator>GRANDIS, Jennifer Rubin</creator><general>American Association for Cancer Research</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7X8</scope></search><sort><creationdate>20020801</creationdate><title>STAT3 activation abrogates growth factor dependence and contributes to head and neck squamous cell carcinoma tumor growth in vivo</title><author>KIJIMA, Taro ; NIWA, Hideo ; STEINMAN, Richard A ; DRENNING, Stephanie D ; GOODING, William E ; WENTZEL, Abbey L ; SICHUAN XI ; GRANDIS, Jennifer Rubin</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-p237t-fdf4dc8aee10b9606b6b71e1fdd5c18c1145bbf80450dcec3067dfa9e501143d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2002</creationdate><topic>Autocrine Communication - genetics</topic><topic>bcl-X Protein</topic><topic>Biological and medical sciences</topic><topic>Carcinoma, Squamous Cell - metabolism</topic><topic>Carcinoma, Squamous Cell - physiopathology</topic><topic>Cell Cycle - genetics</topic><topic>Cell Division - genetics</topic><topic>Cell physiology</topic><topic>Cyclin D1 - genetics</topic><topic>Cyclin D1 - metabolism</topic><topic>DNA-Binding Proteins - genetics</topic><topic>DNA-Binding Proteins - metabolism</topic><topic>Epidermal Growth Factor - metabolism</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Gene Expression Regulation, Neoplastic - genetics</topic><topic>Head and Neck Neoplasms - metabolism</topic><topic>Head and Neck Neoplasms - physiopathology</topic><topic>Humans</topic><topic>Molecular and cellular biology</topic><topic>Proto-Oncogene Proteins c-bcl-2 - genetics</topic><topic>Proto-Oncogene Proteins c-bcl-2 - metabolism</topic><topic>Receptor, Epidermal Growth Factor - genetics</topic><topic>Signal transduction</topic><topic>STAT3 Transcription Factor</topic><topic>Trans-Activators - genetics</topic><topic>Trans-Activators - metabolism</topic><topic>Tumor Cells, Cultured</topic><toplevel>online_resources</toplevel><creatorcontrib>KIJIMA, Taro</creatorcontrib><creatorcontrib>NIWA, Hideo</creatorcontrib><creatorcontrib>STEINMAN, Richard A</creatorcontrib><creatorcontrib>DRENNING, Stephanie D</creatorcontrib><creatorcontrib>GOODING, William E</creatorcontrib><creatorcontrib>WENTZEL, Abbey L</creatorcontrib><creatorcontrib>SICHUAN XI</creatorcontrib><creatorcontrib>GRANDIS, Jennifer Rubin</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>MEDLINE - Academic</collection><jtitle>Cell growth & differentiation</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>KIJIMA, Taro</au><au>NIWA, Hideo</au><au>STEINMAN, Richard A</au><au>DRENNING, Stephanie D</au><au>GOODING, William E</au><au>WENTZEL, Abbey L</au><au>SICHUAN XI</au><au>GRANDIS, Jennifer Rubin</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>STAT3 activation abrogates growth factor dependence and contributes to head and neck squamous cell carcinoma tumor growth in vivo</atitle><jtitle>Cell growth & differentiation</jtitle><addtitle>Cell Growth Differ</addtitle><date>2002-08-01</date><risdate>2002</risdate><volume>13</volume><issue>8</issue><spage>355</spage><epage>362</epage><pages>355-362</pages><issn>1044-9523</issn><abstract>Epidermal growth factor receptor (EGFR) is up-regulated and contributes to the loss of growth control in squamous cell carcinoma of the head and neck (SCCHN). Previously, we reported an association between autocrine stimulation of EGFR and constitutive signal transducers and activators of transcription (STAT) 3 activation in SCCHN cells in vitro and in vivo. Here, we evaluated the role of activated STAT3 in tumor progression and EGFR-independent mitogenic signaling. We found that SCCHN cells stably transfected with a dominant active STAT3 construct expressed elevated levels of STAT3 target genes, including Bcl-X(L) and cyclin D1, and demonstrated increased proliferation in vitro and more rapid tumor growth rates in vivo. Cell cycle analysis demonstrated an increased proportion of STAT3 construct transfectants in G(2)-M. These findings provide evidence that constitutive STAT3 activation contributes to tumor growth in SCCHN, independent of the EGFR autocrine axis.</abstract><cop>Philadelphia, PA</cop><pub>American Association for Cancer Research</pub><pmid>12193474</pmid><tpages>8</tpages></addata></record> |
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| subjects | Autocrine Communication - genetics bcl-X Protein Biological and medical sciences Carcinoma, Squamous Cell - metabolism Carcinoma, Squamous Cell - physiopathology Cell Cycle - genetics Cell Division - genetics Cell physiology Cyclin D1 - genetics Cyclin D1 - metabolism DNA-Binding Proteins - genetics DNA-Binding Proteins - metabolism Epidermal Growth Factor - metabolism Fundamental and applied biological sciences. Psychology Gene Expression Regulation, Neoplastic - genetics Head and Neck Neoplasms - metabolism Head and Neck Neoplasms - physiopathology Humans Molecular and cellular biology Proto-Oncogene Proteins c-bcl-2 - genetics Proto-Oncogene Proteins c-bcl-2 - metabolism Receptor, Epidermal Growth Factor - genetics Signal transduction STAT3 Transcription Factor Trans-Activators - genetics Trans-Activators - metabolism Tumor Cells, Cultured |
| title | STAT3 activation abrogates growth factor dependence and contributes to head and neck squamous cell carcinoma tumor growth in vivo |
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