The role of FOXP3 in the development and metastatic spread of breast cancer
The transcription factor FOXP3 is widely known for its role in the development and function of immunoregulatory T cells. However, it has been discovered recently that FOXP3 is also expressed in epithelial cells of the normal human breast, ovary and prostate. Aggressive cancer of these epithelial tis...
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Veröffentlicht in: | Cancer and metastasis reviews 2012-12, Vol.31 (3-4), p.843-854 |
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description | The transcription factor FOXP3 is widely known for its role in the development and function of immunoregulatory T cells. However, it has been discovered recently that FOXP3 is also expressed in epithelial cells of the normal human breast, ovary and prostate. Aggressive cancer of these epithelial tissues often correlates with abnormal expression of FOXP3, which can be either absent or underexpressed at transcript or protein levels. It is becoming clear that this failure of normal FOXP3 expression can result in dysregulation of the expression of a range of oncogenes which have been implicated in the development and metastasis of cancer. Recent evidence suggests that FOXP3 might also regulate chemokine receptor expression, providing a possible explanation for the chemokine-driven, tissue-specific spread that is characteristic of many cancers. This review first summarises the general structure, function and properties of FOXP3. This is followed by an analysis of the tumour-suppressive properties of this transcription factor, with particular reference to the development and chemokine-mediated spread of human breast cancer. A final section focuses on potential applications of this new knowledge for therapeutic intervention. |
doi_str_mv | 10.1007/s10555-012-9395-3 |
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However, it has been discovered recently that FOXP3 is also expressed in epithelial cells of the normal human breast, ovary and prostate. Aggressive cancer of these epithelial tissues often correlates with abnormal expression of FOXP3, which can be either absent or underexpressed at transcript or protein levels. It is becoming clear that this failure of normal FOXP3 expression can result in dysregulation of the expression of a range of oncogenes which have been implicated in the development and metastasis of cancer. Recent evidence suggests that FOXP3 might also regulate chemokine receptor expression, providing a possible explanation for the chemokine-driven, tissue-specific spread that is characteristic of many cancers. This review first summarises the general structure, function and properties of FOXP3. This is followed by an analysis of the tumour-suppressive properties of this transcription factor, with particular reference to the development and chemokine-mediated spread of human breast cancer. A final section focuses on potential applications of this new knowledge for therapeutic intervention.</description><identifier>ISSN: 0167-7659</identifier><identifier>EISSN: 1573-7233</identifier><identifier>DOI: 10.1007/s10555-012-9395-3</identifier><identifier>PMID: 22833279</identifier><identifier>CODEN: CMRED4</identifier><language>eng</language><publisher>Boston: Springer US</publisher><subject>Analysis ; Animals ; B cells ; Biological and medical sciences ; Biomedical and Life Sciences ; Biomedicine ; Breast cancer ; Breast Neoplasms - chemistry ; Breast Neoplasms - drug therapy ; Breast Neoplasms - etiology ; Breast Neoplasms - pathology ; Cancer Research ; Cell Nucleus - chemistry ; Development and progression ; Female ; Forkhead Transcription Factors - analysis ; Forkhead Transcription Factors - chemistry ; Forkhead Transcription Factors - physiology ; Gene Expression Regulation, Neoplastic ; Genes, Tumor Suppressor ; Gynecology. Andrology. Obstetrics ; Humans ; Mammary gland diseases ; Medical sciences ; Metastasis ; Neoplasm Metastasis ; Non-Thematic Review ; Oncology ; Protein Isoforms - analysis ; T cells ; Tumors ; X Chromosome</subject><ispartof>Cancer and metastasis reviews, 2012-12, Vol.31 (3-4), p.843-854</ispartof><rights>Springer Science+Business Media, LLC 2012</rights><rights>2015 INIST-CNRS</rights><rights>COPYRIGHT 2012 Springer</rights><rights>Springer Science+Business Media New York 2012</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c562t-11a40b9d10a95bd632c296653d52aa0e67f89296266c5bd0420f872c4e7488b03</citedby><cites>FETCH-LOGICAL-c562t-11a40b9d10a95bd632c296653d52aa0e67f89296266c5bd0420f872c4e7488b03</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s10555-012-9395-3$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s10555-012-9395-3$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=26466759$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22833279$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Douglass, Stephen</creatorcontrib><creatorcontrib>Ali, Simi</creatorcontrib><creatorcontrib>Meeson, Annette P.</creatorcontrib><creatorcontrib>Browell, David</creatorcontrib><creatorcontrib>Kirby, John A.</creatorcontrib><title>The role of FOXP3 in the development and metastatic spread of breast cancer</title><title>Cancer and metastasis reviews</title><addtitle>Cancer Metastasis Rev</addtitle><addtitle>Cancer Metastasis Rev</addtitle><description>The transcription factor FOXP3 is widely known for its role in the development and function of immunoregulatory T cells. However, it has been discovered recently that FOXP3 is also expressed in epithelial cells of the normal human breast, ovary and prostate. Aggressive cancer of these epithelial tissues often correlates with abnormal expression of FOXP3, which can be either absent or underexpressed at transcript or protein levels. It is becoming clear that this failure of normal FOXP3 expression can result in dysregulation of the expression of a range of oncogenes which have been implicated in the development and metastasis of cancer. Recent evidence suggests that FOXP3 might also regulate chemokine receptor expression, providing a possible explanation for the chemokine-driven, tissue-specific spread that is characteristic of many cancers. This review first summarises the general structure, function and properties of FOXP3. This is followed by an analysis of the tumour-suppressive properties of this transcription factor, with particular reference to the development and chemokine-mediated spread of human breast cancer. A final section focuses on potential applications of this new knowledge for therapeutic intervention.</description><subject>Analysis</subject><subject>Animals</subject><subject>B cells</subject><subject>Biological and medical sciences</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Breast cancer</subject><subject>Breast Neoplasms - chemistry</subject><subject>Breast Neoplasms - drug therapy</subject><subject>Breast Neoplasms - etiology</subject><subject>Breast Neoplasms - pathology</subject><subject>Cancer Research</subject><subject>Cell Nucleus - chemistry</subject><subject>Development and progression</subject><subject>Female</subject><subject>Forkhead Transcription Factors - analysis</subject><subject>Forkhead Transcription Factors - chemistry</subject><subject>Forkhead Transcription Factors - physiology</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Genes, Tumor Suppressor</subject><subject>Gynecology. Andrology. Obstetrics</subject><subject>Humans</subject><subject>Mammary gland diseases</subject><subject>Medical sciences</subject><subject>Metastasis</subject><subject>Neoplasm Metastasis</subject><subject>Non-Thematic Review</subject><subject>Oncology</subject><subject>Protein Isoforms - analysis</subject><subject>T cells</subject><subject>Tumors</subject><subject>X Chromosome</subject><issn>0167-7659</issn><issn>1573-7233</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNp1kU9vFSEUxYnR2Gf1A7gxRNPEzVT-DDAsm6ZVY5O6qIk7wjB3Ks0MTIFn4reX8T1tNTUsIJffOVzuQeglJceUEPUuUyKEaAhljeZaNPwR2lCheKMY54_RhlCpGiWFPkDPcr4hVcOVfooOGOs4Z0pv0Kerb4BTnADHEZ9ffv3MsQ-41OIA32GKywyhYBsGPEOxudjiHc5LAjusir4ecsHOBgfpOXoy2inDi_1-iL6cn12dfmguLt9_PD25aJyQrDSU2pb0eqDEatEPkjPHtJSCD4JZS0CqsdO1wqR09Z60jIydYq4F1XZdT_ghervzXVK83UIuZvbZwTTZAHGbDaWU8VYQoSv65h_0Jm5TqN2tFFVcKELuqGs7gfFhjCVZt5qaE0VrK4Lw1ev1A5Rb_K25Dx0_ANU1wOxdDDD6Wv_Lle4ELsWcE4xmSX626YehxKwpm13KpqZs1pQNr5pX-19t-xmGP4rfsVbgaA_Y7Ow0ppqPz3ecbKVUv8bDdlxN1IdrSPfG89_XfwLHdLjL</recordid><startdate>20121201</startdate><enddate>20121201</enddate><creator>Douglass, Stephen</creator><creator>Ali, Simi</creator><creator>Meeson, Annette P.</creator><creator>Browell, David</creator><creator>Kirby, John A.</creator><general>Springer US</general><general>Springer</general><general>Springer Nature B.V</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>3V.</scope><scope>7TO</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8FQ</scope><scope>8FV</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>H94</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M3G</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope></search><sort><creationdate>20121201</creationdate><title>The role of FOXP3 in the development and metastatic spread of breast cancer</title><author>Douglass, Stephen ; Ali, Simi ; Meeson, Annette P. ; Browell, David ; Kirby, John A.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c562t-11a40b9d10a95bd632c296653d52aa0e67f89296266c5bd0420f872c4e7488b03</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Analysis</topic><topic>Animals</topic><topic>B cells</topic><topic>Biological and medical sciences</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Breast cancer</topic><topic>Breast Neoplasms - chemistry</topic><topic>Breast Neoplasms - drug therapy</topic><topic>Breast Neoplasms - etiology</topic><topic>Breast Neoplasms - pathology</topic><topic>Cancer Research</topic><topic>Cell Nucleus - chemistry</topic><topic>Development and progression</topic><topic>Female</topic><topic>Forkhead Transcription Factors - analysis</topic><topic>Forkhead Transcription Factors - chemistry</topic><topic>Forkhead Transcription Factors - physiology</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Genes, Tumor Suppressor</topic><topic>Gynecology. Andrology. Obstetrics</topic><topic>Humans</topic><topic>Mammary gland diseases</topic><topic>Medical sciences</topic><topic>Metastasis</topic><topic>Neoplasm Metastasis</topic><topic>Non-Thematic Review</topic><topic>Oncology</topic><topic>Protein Isoforms - analysis</topic><topic>T cells</topic><topic>Tumors</topic><topic>X Chromosome</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Douglass, Stephen</creatorcontrib><creatorcontrib>Ali, Simi</creatorcontrib><creatorcontrib>Meeson, Annette P.</creatorcontrib><creatorcontrib>Browell, David</creatorcontrib><creatorcontrib>Kirby, John A.</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>ProQuest Central (Corporate)</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Canadian Business & Current Affairs Database</collection><collection>Canadian Business & Current Affairs Database (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>CBCA Reference & Current Events</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><jtitle>Cancer and metastasis reviews</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Douglass, Stephen</au><au>Ali, Simi</au><au>Meeson, Annette P.</au><au>Browell, David</au><au>Kirby, John A.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The role of FOXP3 in the development and metastatic spread of breast cancer</atitle><jtitle>Cancer and metastasis reviews</jtitle><stitle>Cancer Metastasis Rev</stitle><addtitle>Cancer Metastasis Rev</addtitle><date>2012-12-01</date><risdate>2012</risdate><volume>31</volume><issue>3-4</issue><spage>843</spage><epage>854</epage><pages>843-854</pages><issn>0167-7659</issn><eissn>1573-7233</eissn><coden>CMRED4</coden><abstract>The transcription factor FOXP3 is widely known for its role in the development and function of immunoregulatory T cells. However, it has been discovered recently that FOXP3 is also expressed in epithelial cells of the normal human breast, ovary and prostate. Aggressive cancer of these epithelial tissues often correlates with abnormal expression of FOXP3, which can be either absent or underexpressed at transcript or protein levels. It is becoming clear that this failure of normal FOXP3 expression can result in dysregulation of the expression of a range of oncogenes which have been implicated in the development and metastasis of cancer. Recent evidence suggests that FOXP3 might also regulate chemokine receptor expression, providing a possible explanation for the chemokine-driven, tissue-specific spread that is characteristic of many cancers. This review first summarises the general structure, function and properties of FOXP3. This is followed by an analysis of the tumour-suppressive properties of this transcription factor, with particular reference to the development and chemokine-mediated spread of human breast cancer. A final section focuses on potential applications of this new knowledge for therapeutic intervention.</abstract><cop>Boston</cop><pub>Springer US</pub><pmid>22833279</pmid><doi>10.1007/s10555-012-9395-3</doi><tpages>12</tpages></addata></record> |
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subjects | Analysis Animals B cells Biological and medical sciences Biomedical and Life Sciences Biomedicine Breast cancer Breast Neoplasms - chemistry Breast Neoplasms - drug therapy Breast Neoplasms - etiology Breast Neoplasms - pathology Cancer Research Cell Nucleus - chemistry Development and progression Female Forkhead Transcription Factors - analysis Forkhead Transcription Factors - chemistry Forkhead Transcription Factors - physiology Gene Expression Regulation, Neoplastic Genes, Tumor Suppressor Gynecology. Andrology. Obstetrics Humans Mammary gland diseases Medical sciences Metastasis Neoplasm Metastasis Non-Thematic Review Oncology Protein Isoforms - analysis T cells Tumors X Chromosome |
title | The role of FOXP3 in the development and metastatic spread of breast cancer |
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