Twist overexpression induces in vivo angiogenesis and correlates with chromosomal instability in breast cancer
Aggressive cancer phenotypes are a manifestation of many different genetic alterations that promote rapid proliferation and metastasis. In this study, we show that stable overexpression of Twist in a breast cancer cell line, MCF-7, altered its morphology to a fibroblastic-like phenotype, which exhib...
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| Veröffentlicht in: | Cancer research (Chicago, Ill.) Ill.), 2005-12, Vol.65 (23), p.10801-10809 |
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| creator | MIRONCHIK, Yelena WINNARD, Paul T BURGER, Horst GLACKIN, Carlotta RAMAN, Venu VESUNA, Farhad KATO, Yoshinori WILDES, Flonne PATHAK, Arvind P KOMINSKY, Scott ARTEMOV, Dmitri BHUJWALLA, Zaver VAN DIEST, Paul |
| description | Aggressive cancer phenotypes are a manifestation of many different genetic alterations that promote rapid proliferation and metastasis. In this study, we show that stable overexpression of Twist in a breast cancer cell line, MCF-7, altered its morphology to a fibroblastic-like phenotype, which exhibited protein markers representative of a mesenchymal transformation. In addition, it was observed that MCF-7/Twist cells had increased vascular endothelial growth factor (VEGF) synthesis when compared with empty vector control cells. The functional changes induced by VEGF in vivo were analyzed by functional magnetic resonance imaging (MRI) of MCF-7/Twist-xenografted tumors. MRI showed that MCF-7/Twist tumors exhibited higher vascular volume and vascular permeability in vivo than the MCF-7/vector control xenografts. Moreover, elevated expression of Twist in breast tumor samples obtained from patients correlated strongly with high-grade invasive carcinomas and with chromosome instability, particularly gains of chromosomes 1 and 7. Taken together, these results show that Twist overexpression in breast cancer cells can induce angiogenesis, correlates with chromosomal instability, and promotes an epithelial-mesenchymal-like transition that is pivotal for the transformation into an aggressive breast cancer phenotype. |
| doi_str_mv | 10.1158/0008-5472.CAN-05-0712 |
| format | Article |
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In this study, we show that stable overexpression of Twist in a breast cancer cell line, MCF-7, altered its morphology to a fibroblastic-like phenotype, which exhibited protein markers representative of a mesenchymal transformation. In addition, it was observed that MCF-7/Twist cells had increased vascular endothelial growth factor (VEGF) synthesis when compared with empty vector control cells. The functional changes induced by VEGF in vivo were analyzed by functional magnetic resonance imaging (MRI) of MCF-7/Twist-xenografted tumors. MRI showed that MCF-7/Twist tumors exhibited higher vascular volume and vascular permeability in vivo than the MCF-7/vector control xenografts. Moreover, elevated expression of Twist in breast tumor samples obtained from patients correlated strongly with high-grade invasive carcinomas and with chromosome instability, particularly gains of chromosomes 1 and 7. Taken together, these results show that Twist overexpression in breast cancer cells can induce angiogenesis, correlates with chromosomal instability, and promotes an epithelial-mesenchymal-like transition that is pivotal for the transformation into an aggressive breast cancer phenotype.</description><identifier>ISSN: 0008-5472</identifier><identifier>EISSN: 1538-7445</identifier><identifier>DOI: 10.1158/0008-5472.CAN-05-0712</identifier><identifier>PMID: 16322226</identifier><identifier>CODEN: CNREA8</identifier><language>eng</language><publisher>Philadelphia, PA: American Association for Cancer Research</publisher><subject>Animals ; Biological and medical sciences ; Breast Neoplasms - blood supply ; Breast Neoplasms - genetics ; Breast Neoplasms - metabolism ; Breast Neoplasms - pathology ; Capillary Permeability - physiology ; Cell Growth Processes - physiology ; Cell Line, Tumor ; Cell Movement - physiology ; Chromosomal Instability ; Claudins ; Dissemination ; Female ; Gynecology. Andrology. Obstetrics ; Humans ; Mammary gland diseases ; Medical sciences ; Membrane Proteins - genetics ; Mesoderm - metabolism ; Mice ; Mice, SCID ; Neoplasm Invasiveness ; Neoplasm Transplantation ; Neovascularization, Pathologic - genetics ; Neovascularization, Pathologic - metabolism ; Neovascularization, Pathologic - pathology ; Nuclear Proteins - biosynthesis ; Transcriptional Activation ; Transplantation, Heterologous ; Tumor cell ; Tumors ; Twist-Related Protein 1 - biosynthesis</subject><ispartof>Cancer research (Chicago, Ill.), 2005-12, Vol.65 (23), p.10801-10809</ispartof><rights>2006 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c505t-f2e1ea405d2d05c0ef504c1ceb7c8f86f1ca499ddb69c91adc22b13fff38a25b3</citedby><cites>FETCH-LOGICAL-c505t-f2e1ea405d2d05c0ef504c1ceb7c8f86f1ca499ddb69c91adc22b13fff38a25b3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,776,780,881,3343,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=17313430$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16322226$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>MIRONCHIK, Yelena</creatorcontrib><creatorcontrib>WINNARD, Paul T</creatorcontrib><creatorcontrib>BURGER, Horst</creatorcontrib><creatorcontrib>GLACKIN, Carlotta</creatorcontrib><creatorcontrib>RAMAN, Venu</creatorcontrib><creatorcontrib>VESUNA, Farhad</creatorcontrib><creatorcontrib>KATO, Yoshinori</creatorcontrib><creatorcontrib>WILDES, Flonne</creatorcontrib><creatorcontrib>PATHAK, Arvind P</creatorcontrib><creatorcontrib>KOMINSKY, Scott</creatorcontrib><creatorcontrib>ARTEMOV, Dmitri</creatorcontrib><creatorcontrib>BHUJWALLA, Zaver</creatorcontrib><creatorcontrib>VAN DIEST, Paul</creatorcontrib><title>Twist overexpression induces in vivo angiogenesis and correlates with chromosomal instability in breast cancer</title><title>Cancer research (Chicago, Ill.)</title><addtitle>Cancer Res</addtitle><description>Aggressive cancer phenotypes are a manifestation of many different genetic alterations that promote rapid proliferation and metastasis. In this study, we show that stable overexpression of Twist in a breast cancer cell line, MCF-7, altered its morphology to a fibroblastic-like phenotype, which exhibited protein markers representative of a mesenchymal transformation. In addition, it was observed that MCF-7/Twist cells had increased vascular endothelial growth factor (VEGF) synthesis when compared with empty vector control cells. The functional changes induced by VEGF in vivo were analyzed by functional magnetic resonance imaging (MRI) of MCF-7/Twist-xenografted tumors. MRI showed that MCF-7/Twist tumors exhibited higher vascular volume and vascular permeability in vivo than the MCF-7/vector control xenografts. Moreover, elevated expression of Twist in breast tumor samples obtained from patients correlated strongly with high-grade invasive carcinomas and with chromosome instability, particularly gains of chromosomes 1 and 7. Taken together, these results show that Twist overexpression in breast cancer cells can induce angiogenesis, correlates with chromosomal instability, and promotes an epithelial-mesenchymal-like transition that is pivotal for the transformation into an aggressive breast cancer phenotype.</description><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Breast Neoplasms - blood supply</subject><subject>Breast Neoplasms - genetics</subject><subject>Breast Neoplasms - metabolism</subject><subject>Breast Neoplasms - pathology</subject><subject>Capillary Permeability - physiology</subject><subject>Cell Growth Processes - physiology</subject><subject>Cell Line, Tumor</subject><subject>Cell Movement - physiology</subject><subject>Chromosomal Instability</subject><subject>Claudins</subject><subject>Dissemination</subject><subject>Female</subject><subject>Gynecology. Andrology. Obstetrics</subject><subject>Humans</subject><subject>Mammary gland diseases</subject><subject>Medical sciences</subject><subject>Membrane Proteins - genetics</subject><subject>Mesoderm - metabolism</subject><subject>Mice</subject><subject>Mice, SCID</subject><subject>Neoplasm Invasiveness</subject><subject>Neoplasm Transplantation</subject><subject>Neovascularization, Pathologic - genetics</subject><subject>Neovascularization, Pathologic - metabolism</subject><subject>Neovascularization, Pathologic - pathology</subject><subject>Nuclear Proteins - biosynthesis</subject><subject>Transcriptional Activation</subject><subject>Transplantation, Heterologous</subject><subject>Tumor cell</subject><subject>Tumors</subject><subject>Twist-Related Protein 1 - biosynthesis</subject><issn>0008-5472</issn><issn>1538-7445</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkU1v1DAQhi0EotvCTwDlArcUf03svSBVKyhIFVzK2XKc8a5RYi92dkv_PY66auGEL6ORn3n98RDyhtFLxkB_oJTqFqTil5urby2FlirGn5EVA6FbJSU8J6tH5oycl_KztsAovCRnrBO8rm5F4u1dKHOTjpjx9z5jKSHFJsTh4LDU2hzDMTU2bkPaYsQSSm2GxqWccbRzZe7CvGvcLqcplTTZsQ6V2fZhDPP9EtBntPUEZ6PD_Iq88HYs-PpUL8iPz59uN1_am-_XXzdXN60DCnPrOTK0ksLABwqOogcqHXPYK6e97jxzVq7Xw9B3a7dmdnCc90x474W2HHpxQT4-5O4P_YSDwzhnO5p9DpPN9ybZYP7diWFntuloABRormvA-1NATr8OWGYzheJwHG3EdCim0xok7br_gkxJ3oFSFYQH0OVUSkb_eBtGzaLULLrMostUpYaCWZTWubd_P-Vp6uSwAu9OgC3Ojj7Xnw7liVOCCSmo-AMzyq6w</recordid><startdate>20051201</startdate><enddate>20051201</enddate><creator>MIRONCHIK, Yelena</creator><creator>WINNARD, Paul T</creator><creator>BURGER, Horst</creator><creator>GLACKIN, Carlotta</creator><creator>RAMAN, Venu</creator><creator>VESUNA, Farhad</creator><creator>KATO, Yoshinori</creator><creator>WILDES, Flonne</creator><creator>PATHAK, Arvind P</creator><creator>KOMINSKY, Scott</creator><creator>ARTEMOV, Dmitri</creator><creator>BHUJWALLA, Zaver</creator><creator>VAN DIEST, Paul</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>7TO</scope><scope>8FD</scope><scope>FR3</scope><scope>H94</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20051201</creationdate><title>Twist overexpression induces in vivo angiogenesis and correlates with chromosomal instability in breast cancer</title><author>MIRONCHIK, Yelena ; WINNARD, Paul T ; BURGER, Horst ; GLACKIN, Carlotta ; RAMAN, Venu ; VESUNA, Farhad ; KATO, Yoshinori ; WILDES, Flonne ; PATHAK, Arvind P ; KOMINSKY, Scott ; ARTEMOV, Dmitri ; BHUJWALLA, Zaver ; VAN DIEST, Paul</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c505t-f2e1ea405d2d05c0ef504c1ceb7c8f86f1ca499ddb69c91adc22b13fff38a25b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Breast Neoplasms - blood supply</topic><topic>Breast Neoplasms - genetics</topic><topic>Breast Neoplasms - metabolism</topic><topic>Breast Neoplasms - pathology</topic><topic>Capillary Permeability - physiology</topic><topic>Cell Growth Processes - physiology</topic><topic>Cell Line, Tumor</topic><topic>Cell Movement - physiology</topic><topic>Chromosomal Instability</topic><topic>Claudins</topic><topic>Dissemination</topic><topic>Female</topic><topic>Gynecology. Andrology. Obstetrics</topic><topic>Humans</topic><topic>Mammary gland diseases</topic><topic>Medical sciences</topic><topic>Membrane Proteins - genetics</topic><topic>Mesoderm - metabolism</topic><topic>Mice</topic><topic>Mice, SCID</topic><topic>Neoplasm Invasiveness</topic><topic>Neoplasm Transplantation</topic><topic>Neovascularization, Pathologic - genetics</topic><topic>Neovascularization, Pathologic - metabolism</topic><topic>Neovascularization, Pathologic - pathology</topic><topic>Nuclear Proteins - biosynthesis</topic><topic>Transcriptional Activation</topic><topic>Transplantation, Heterologous</topic><topic>Tumor cell</topic><topic>Tumors</topic><topic>Twist-Related Protein 1 - biosynthesis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>MIRONCHIK, Yelena</creatorcontrib><creatorcontrib>WINNARD, Paul T</creatorcontrib><creatorcontrib>BURGER, Horst</creatorcontrib><creatorcontrib>GLACKIN, Carlotta</creatorcontrib><creatorcontrib>RAMAN, Venu</creatorcontrib><creatorcontrib>VESUNA, Farhad</creatorcontrib><creatorcontrib>KATO, Yoshinori</creatorcontrib><creatorcontrib>WILDES, Flonne</creatorcontrib><creatorcontrib>PATHAK, Arvind P</creatorcontrib><creatorcontrib>KOMINSKY, Scott</creatorcontrib><creatorcontrib>ARTEMOV, Dmitri</creatorcontrib><creatorcontrib>BHUJWALLA, Zaver</creatorcontrib><creatorcontrib>VAN DIEST, Paul</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>Oncogenes and Growth Factors Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</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>MIRONCHIK, Yelena</au><au>WINNARD, Paul T</au><au>BURGER, Horst</au><au>GLACKIN, Carlotta</au><au>RAMAN, Venu</au><au>VESUNA, Farhad</au><au>KATO, Yoshinori</au><au>WILDES, Flonne</au><au>PATHAK, Arvind P</au><au>KOMINSKY, Scott</au><au>ARTEMOV, Dmitri</au><au>BHUJWALLA, Zaver</au><au>VAN DIEST, Paul</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Twist overexpression induces in vivo angiogenesis and correlates with chromosomal instability in breast cancer</atitle><jtitle>Cancer research (Chicago, Ill.)</jtitle><addtitle>Cancer Res</addtitle><date>2005-12-01</date><risdate>2005</risdate><volume>65</volume><issue>23</issue><spage>10801</spage><epage>10809</epage><pages>10801-10809</pages><issn>0008-5472</issn><eissn>1538-7445</eissn><coden>CNREA8</coden><abstract>Aggressive cancer phenotypes are a manifestation of many different genetic alterations that promote rapid proliferation and metastasis. In this study, we show that stable overexpression of Twist in a breast cancer cell line, MCF-7, altered its morphology to a fibroblastic-like phenotype, which exhibited protein markers representative of a mesenchymal transformation. In addition, it was observed that MCF-7/Twist cells had increased vascular endothelial growth factor (VEGF) synthesis when compared with empty vector control cells. The functional changes induced by VEGF in vivo were analyzed by functional magnetic resonance imaging (MRI) of MCF-7/Twist-xenografted tumors. MRI showed that MCF-7/Twist tumors exhibited higher vascular volume and vascular permeability in vivo than the MCF-7/vector control xenografts. Moreover, elevated expression of Twist in breast tumor samples obtained from patients correlated strongly with high-grade invasive carcinomas and with chromosome instability, particularly gains of chromosomes 1 and 7. Taken together, these results show that Twist overexpression in breast cancer cells can induce angiogenesis, correlates with chromosomal instability, and promotes an epithelial-mesenchymal-like transition that is pivotal for the transformation into an aggressive breast cancer phenotype.</abstract><cop>Philadelphia, PA</cop><pub>American Association for Cancer Research</pub><pmid>16322226</pmid><doi>10.1158/0008-5472.CAN-05-0712</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Cancer research (Chicago, Ill.), 2005-12, Vol.65 (23), p.10801-10809 |
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| source | MEDLINE; American Association for Cancer Research; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals |
| subjects | Animals Biological and medical sciences Breast Neoplasms - blood supply Breast Neoplasms - genetics Breast Neoplasms - metabolism Breast Neoplasms - pathology Capillary Permeability - physiology Cell Growth Processes - physiology Cell Line, Tumor Cell Movement - physiology Chromosomal Instability Claudins Dissemination Female Gynecology. Andrology. Obstetrics Humans Mammary gland diseases Medical sciences Membrane Proteins - genetics Mesoderm - metabolism Mice Mice, SCID Neoplasm Invasiveness Neoplasm Transplantation Neovascularization, Pathologic - genetics Neovascularization, Pathologic - metabolism Neovascularization, Pathologic - pathology Nuclear Proteins - biosynthesis Transcriptional Activation Transplantation, Heterologous Tumor cell Tumors Twist-Related Protein 1 - biosynthesis |
| title | Twist overexpression induces in vivo angiogenesis and correlates with chromosomal instability in breast cancer |
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