Identification of a Stat3-Dependent Transcription Regulatory Network Involved in Metastatic Progression
High levels of activated Stat3 are often found in human breast cancers and can correlate with poor patient outcome. We employed an activated ErbB2 mouse model of breast cancer to investigate the in vivo role of Stat3 in mammary tumor progression and found that Stat3 does not alter mammary tumor init...
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| Veröffentlicht in: | Cancer research (Chicago, Ill.) Ill.), 2009-09, Vol.69 (17), p.6823-6830 |
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| container_title | Cancer research (Chicago, Ill.) |
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| creator | RANGER, Jill J LEVY, David E SHAHALIZADEH, Solmaz HALLETT, Michael MULLER, William J |
| description | High levels of activated Stat3 are often found in human breast cancers and can correlate with poor patient outcome. We employed an activated ErbB2 mouse model of breast cancer to investigate the in vivo role of Stat3 in mammary tumor progression and found that Stat3 does not alter mammary tumor initiation but dramatically affects metastatic progression. Four-fold fewer animals exhibited lung metastases in the absence of Stat3 and a 12-fold reduction in the number of lung lesions was observed in animals bearing Stat3-null tumors when compared with the wild-type cohort. The decreased malignancy in Stat3-deficient tumors is attributed to a reduction in both angiogenic and inflammatory responses associated with a Stat3-dependent transcriptional cascade involving CCAAT/enhancer binding protein delta. |
| doi_str_mv | 10.1158/0008-5472.CAN-09-1684 |
| format | Article |
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We employed an activated ErbB2 mouse model of breast cancer to investigate the in vivo role of Stat3 in mammary tumor progression and found that Stat3 does not alter mammary tumor initiation but dramatically affects metastatic progression. Four-fold fewer animals exhibited lung metastases in the absence of Stat3 and a 12-fold reduction in the number of lung lesions was observed in animals bearing Stat3-null tumors when compared with the wild-type cohort. The decreased malignancy in Stat3-deficient tumors is attributed to a reduction in both angiogenic and inflammatory responses associated with a Stat3-dependent transcriptional cascade involving CCAAT/enhancer binding protein delta.</description><identifier>ISSN: 0008-5472</identifier><identifier>EISSN: 1538-7445</identifier><identifier>DOI: 10.1158/0008-5472.CAN-09-1684</identifier><identifier>PMID: 19690134</identifier><identifier>CODEN: CNREA8</identifier><language>eng</language><publisher>Philadelphia, PA: American Association for Cancer Research</publisher><subject>Animals ; Antineoplastic agents ; Biological and medical sciences ; CCAAT-Enhancer-Binding Protein-delta - genetics ; CCAAT-Enhancer-Binding Protein-delta - metabolism ; Cell Transformation, Neoplastic ; Female ; Gynecology. Andrology. Obstetrics ; Humans ; Lung Neoplasms - genetics ; Lung Neoplasms - secondary ; Mammary gland diseases ; Mammary Neoplasms, Animal - genetics ; Mammary Neoplasms, Animal - pathology ; Medical sciences ; Mice ; Mice, Transgenic ; Neoplasm Invasiveness - genetics ; Neovascularization, Pathologic - genetics ; Pharmacology. 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We employed an activated ErbB2 mouse model of breast cancer to investigate the in vivo role of Stat3 in mammary tumor progression and found that Stat3 does not alter mammary tumor initiation but dramatically affects metastatic progression. Four-fold fewer animals exhibited lung metastases in the absence of Stat3 and a 12-fold reduction in the number of lung lesions was observed in animals bearing Stat3-null tumors when compared with the wild-type cohort. The decreased malignancy in Stat3-deficient tumors is attributed to a reduction in both angiogenic and inflammatory responses associated with a Stat3-dependent transcriptional cascade involving CCAAT/enhancer binding protein delta.</description><subject>Animals</subject><subject>Antineoplastic agents</subject><subject>Biological and medical sciences</subject><subject>CCAAT-Enhancer-Binding Protein-delta - genetics</subject><subject>CCAAT-Enhancer-Binding Protein-delta - metabolism</subject><subject>Cell Transformation, Neoplastic</subject><subject>Female</subject><subject>Gynecology. Andrology. Obstetrics</subject><subject>Humans</subject><subject>Lung Neoplasms - genetics</subject><subject>Lung Neoplasms - secondary</subject><subject>Mammary gland diseases</subject><subject>Mammary Neoplasms, Animal - genetics</subject><subject>Mammary Neoplasms, Animal - pathology</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Mice, Transgenic</subject><subject>Neoplasm Invasiveness - genetics</subject><subject>Neovascularization, Pathologic - genetics</subject><subject>Pharmacology. Drug treatments</subject><subject>Receptor, ErbB-2 - genetics</subject><subject>Receptor, ErbB-2 - metabolism</subject><subject>STAT3 Transcription Factor - biosynthesis</subject><subject>STAT3 Transcription Factor - genetics</subject><subject>Transcription, Genetic</subject><subject>Tumors</subject><issn>0008-5472</issn><issn>1538-7445</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpVkMtOAyEUhonR2Hp5BA0bl6MwQAc2Jk29NanVeFkTBpiKTocGpjW-vYxtqq5OyH85hw-AE4zOMWb8AiHEM0aL_Hw0nGZIZHjA6Q7oY0Z4VlDKdkF_6-mBgxjf05NhxPZBD4uBQJjQPpiNjW1aVzmtWucb6Cuo4HOrWpJd2YVtOhW-BNVEHdzix_JkZ8tatT58waltP334gONm5euVNdA18N62KqYCp-Fj8LNgY0ypI7BXqTra4808BK831y-ju2zycDseDSeZZkS0GRdFgbClhoky_UEZggeMFMYWpUG4KBHjPNe0ogPeCUhgpLXVubElMUpocggu172LZTm3Rqfzg6rlIri5Cl_SKyf_K417kzO_kjmnWHCWCti6QAcfY7DVNouR7MjLjqrsqMpEXiIhO_Ipd_p38W9qgzoZzjYGFbWqq8RUu7j15TkmgueEfAMbn48R</recordid><startdate>20090901</startdate><enddate>20090901</enddate><creator>RANGER, Jill J</creator><creator>LEVY, David E</creator><creator>SHAHALIZADEH, Solmaz</creator><creator>HALLETT, Michael</creator><creator>MULLER, William J</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>AAYXX</scope><scope>CITATION</scope><scope>5PM</scope></search><sort><creationdate>20090901</creationdate><title>Identification of a Stat3-Dependent Transcription Regulatory Network Involved in Metastatic Progression</title><author>RANGER, Jill J ; LEVY, David E ; SHAHALIZADEH, Solmaz ; HALLETT, Michael ; MULLER, William J</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c539t-897701e4d59b445ad316537de7bd017b05882c4f46816530910ccec2deb3da9c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2009</creationdate><topic>Animals</topic><topic>Antineoplastic agents</topic><topic>Biological and medical sciences</topic><topic>CCAAT-Enhancer-Binding Protein-delta - genetics</topic><topic>CCAAT-Enhancer-Binding Protein-delta - metabolism</topic><topic>Cell Transformation, Neoplastic</topic><topic>Female</topic><topic>Gynecology. Andrology. Obstetrics</topic><topic>Humans</topic><topic>Lung Neoplasms - genetics</topic><topic>Lung Neoplasms - secondary</topic><topic>Mammary gland diseases</topic><topic>Mammary Neoplasms, Animal - genetics</topic><topic>Mammary Neoplasms, Animal - pathology</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>Mice, Transgenic</topic><topic>Neoplasm Invasiveness - genetics</topic><topic>Neovascularization, Pathologic - genetics</topic><topic>Pharmacology. Drug treatments</topic><topic>Receptor, ErbB-2 - genetics</topic><topic>Receptor, ErbB-2 - metabolism</topic><topic>STAT3 Transcription Factor - biosynthesis</topic><topic>STAT3 Transcription Factor - genetics</topic><topic>Transcription, Genetic</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>RANGER, Jill J</creatorcontrib><creatorcontrib>LEVY, David E</creatorcontrib><creatorcontrib>SHAHALIZADEH, Solmaz</creatorcontrib><creatorcontrib>HALLETT, Michael</creatorcontrib><creatorcontrib>MULLER, William J</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>PubMed Central (Full Participant titles)</collection><jtitle>Cancer research (Chicago, Ill.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>RANGER, Jill J</au><au>LEVY, David E</au><au>SHAHALIZADEH, Solmaz</au><au>HALLETT, Michael</au><au>MULLER, William J</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Identification of a Stat3-Dependent Transcription Regulatory Network Involved in Metastatic Progression</atitle><jtitle>Cancer research (Chicago, Ill.)</jtitle><addtitle>Cancer Res</addtitle><date>2009-09-01</date><risdate>2009</risdate><volume>69</volume><issue>17</issue><spage>6823</spage><epage>6830</epage><pages>6823-6830</pages><issn>0008-5472</issn><eissn>1538-7445</eissn><coden>CNREA8</coden><abstract>High levels of activated Stat3 are often found in human breast cancers and can correlate with poor patient outcome. 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| ispartof | Cancer research (Chicago, Ill.), 2009-09, Vol.69 (17), p.6823-6830 |
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| source | MEDLINE; American Association for Cancer Research; EZB-FREE-00999 freely available EZB journals |
| subjects | Animals Antineoplastic agents Biological and medical sciences CCAAT-Enhancer-Binding Protein-delta - genetics CCAAT-Enhancer-Binding Protein-delta - metabolism Cell Transformation, Neoplastic Female Gynecology. Andrology. Obstetrics Humans Lung Neoplasms - genetics Lung Neoplasms - secondary Mammary gland diseases Mammary Neoplasms, Animal - genetics Mammary Neoplasms, Animal - pathology Medical sciences Mice Mice, Transgenic Neoplasm Invasiveness - genetics Neovascularization, Pathologic - genetics Pharmacology. Drug treatments Receptor, ErbB-2 - genetics Receptor, ErbB-2 - metabolism STAT3 Transcription Factor - biosynthesis STAT3 Transcription Factor - genetics Transcription, Genetic Tumors |
| title | Identification of a Stat3-Dependent Transcription Regulatory Network Involved in Metastatic Progression |
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