LymphedemaV1, Pmc, Corpus, bibRecord, 002765

The Foxc2 transcription factor regulates tumor angiogenesis

Identifieur interne : 002765 ( Pmc/Corpus ); précédent : 002764; suivant : 002766

The Foxc2 transcription factor regulates tumor angiogenesis

Auteurs : Hideto Sano ; Jared P. Leboeuf ; Sergey V. Novitsky ; Seungwoon Seo ; Snjezana Zaja-Milatovic ; Mikhail M. Dikov ; Tsutomu Kume

Source :

Biochemical and biophysical research communications [ 0006-291X ] ; 2010.

RBID : PMC:2822046

Abstract

The Forkhead/Fox transcription factor Foxc2 is a critical regulator of vascular development. However, the role of Foxc2 in pathological angiogenesis in cancer remains unknown. Here we show that FoxC2 is highly expressed in human breast and colonic tumors and in the tumor endothelium in human and mouse melanomas. Using the B16 melanoma tumor model, we investigated the function of Foxc2 in tumor angiogenesis. After subcutaneous injection of B16 melanoma cells, primary tumor growth as well as neovascularization was markedly reduced in mice lacking one copy of the Foxc2 gene (Foxc2+/-). Consistently, expression levels of several angiogenic factors, including vascular endothelial growth factor (Vegf), matrix metallopeptidase 2 (Mmp2), and platelet-derived growth factor-B (Pdgfb), were significantly decreased in B16 tumors grown in Foxc2+/- mice, and tumor blood vessels formed in Foxc2+/- mice showed reduced coverage of mural cells and endothelial cell apoptosis. In addition, the tumor tissue in Foxc2+/- mice had an accumulation of necrotic cells. Taken together, these findings demonstrate that haplodeficiency of Foxc2 results in impaired formation of tumor blood vessels as well as reduced tumor growth and thereby provide evidence that Foxc2 is critical for tumor development and angiogenesis.

Url:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2822046

DOI: 10.1016/j.bbrc.2010.01.015
PubMed: 20060810
PubMed Central: 2822046

Links to Exploration step

PMC:2822046

Le document en format XML

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<author><name sortKey="Sano, Hideto" sort="Sano, Hideto" uniqKey="Sano H" first="Hideto" last="Sano">Hideto Sano</name>
<affiliation><nlm:aff id="A1">Division of Cardiovascular Medicine, Department of Medicine, Vanderbilt University Medical Center, 2220 Pierce Ave, Nashville, TN 37232-6300, USA</nlm:aff>
</affiliation>
</author>
<author><name sortKey="Leboeuf, Jared P" sort="Leboeuf, Jared P" uniqKey="Leboeuf J" first="Jared P" last="Leboeuf">Jared P. Leboeuf</name>
<affiliation><nlm:aff id="A1">Division of Cardiovascular Medicine, Department of Medicine, Vanderbilt University Medical Center, 2220 Pierce Ave, Nashville, TN 37232-6300, USA</nlm:aff>
</affiliation>
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<author><name sortKey="Novitsky, Sergey V" sort="Novitsky, Sergey V" uniqKey="Novitsky S" first="Sergey V" last="Novitsky">Sergey V. Novitsky</name>
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</affiliation>
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<author><name sortKey="Seo, Seungwoon" sort="Seo, Seungwoon" uniqKey="Seo S" first="Seungwoon" last="Seo">Seungwoon Seo</name>
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</affiliation>
</author>
<author><name sortKey="Zaja Milatovic, Snjezana" sort="Zaja Milatovic, Snjezana" uniqKey="Zaja Milatovic S" first="Snjezana" last="Zaja-Milatovic">Snjezana Zaja-Milatovic</name>
<affiliation><nlm:aff id="A2">Hematology Oncology, Department of Medicine, Vanderbilt University Medical Center, 2220 Pierce Ave, Nashville, TN 37232-6300, USA</nlm:aff>
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<author><name sortKey="Dikov, Mikhail M" sort="Dikov, Mikhail M" uniqKey="Dikov M" first="Mikhail M." last="Dikov">Mikhail M. Dikov</name>
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</affiliation>
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<author><name sortKey="Kume, Tsutomu" sort="Kume, Tsutomu" uniqKey="Kume T" first="Tsutomu" last="Kume">Tsutomu Kume</name>
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<author><name sortKey="Leboeuf, Jared P" sort="Leboeuf, Jared P" uniqKey="Leboeuf J" first="Jared P" last="Leboeuf">Jared P. Leboeuf</name>
<affiliation><nlm:aff id="A1">Division of Cardiovascular Medicine, Department of Medicine, Vanderbilt University Medical Center, 2220 Pierce Ave, Nashville, TN 37232-6300, USA</nlm:aff>
</affiliation>
</author>
<author><name sortKey="Novitsky, Sergey V" sort="Novitsky, Sergey V" uniqKey="Novitsky S" first="Sergey V" last="Novitsky">Sergey V. Novitsky</name>
<affiliation><nlm:aff id="A2">Hematology Oncology, Department of Medicine, Vanderbilt University Medical Center, 2220 Pierce Ave, Nashville, TN 37232-6300, USA</nlm:aff>
</affiliation>
</author>
<author><name sortKey="Seo, Seungwoon" sort="Seo, Seungwoon" uniqKey="Seo S" first="Seungwoon" last="Seo">Seungwoon Seo</name>
<affiliation><nlm:aff id="A1">Division of Cardiovascular Medicine, Department of Medicine, Vanderbilt University Medical Center, 2220 Pierce Ave, Nashville, TN 37232-6300, USA</nlm:aff>
</affiliation>
</author>
<author><name sortKey="Zaja Milatovic, Snjezana" sort="Zaja Milatovic, Snjezana" uniqKey="Zaja Milatovic S" first="Snjezana" last="Zaja-Milatovic">Snjezana Zaja-Milatovic</name>
<affiliation><nlm:aff id="A2">Hematology Oncology, Department of Medicine, Vanderbilt University Medical Center, 2220 Pierce Ave, Nashville, TN 37232-6300, USA</nlm:aff>
</affiliation>
</author>
<author><name sortKey="Dikov, Mikhail M" sort="Dikov, Mikhail M" uniqKey="Dikov M" first="Mikhail M." last="Dikov">Mikhail M. Dikov</name>
<affiliation><nlm:aff id="A2">Hematology Oncology, Department of Medicine, Vanderbilt University Medical Center, 2220 Pierce Ave, Nashville, TN 37232-6300, USA</nlm:aff>
</affiliation>
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<author><name sortKey="Kume, Tsutomu" sort="Kume, Tsutomu" uniqKey="Kume T" first="Tsutomu" last="Kume">Tsutomu Kume</name>
<affiliation><nlm:aff id="A1">Division of Cardiovascular Medicine, Department of Medicine, Vanderbilt University Medical Center, 2220 Pierce Ave, Nashville, TN 37232-6300, USA</nlm:aff>
</affiliation>
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<series><title level="j">Biochemical and biophysical research communications</title>
<idno type="ISSN">0006-291X</idno>
<idno type="eISSN">1090-2104</idno>
<imprint><date when="2010">2010</date>
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<front><div type="abstract" xml:lang="en"><p id="P1">The Forkhead/Fox transcription factor Foxc2 is a critical regulator of vascular development. However, the role of Foxc2 in pathological angiogenesis in cancer remains unknown. Here we show that FoxC2 is highly expressed in human breast and colonic tumors and in the tumor endothelium in human and mouse melanomas. Using the B16 melanoma tumor model, we investigated the function of Foxc2 in tumor angiogenesis. After subcutaneous injection of B16 melanoma cells, primary tumor growth as well as neovascularization was markedly reduced in mice lacking one copy of the <italic>Foxc2</italic>
 gene (<italic>Foxc2</italic>
+/-). Consistently, expression levels of several angiogenic factors, including <italic>vascular endothelial growth factor</italic>
 (<italic>Vegf</italic>
), <italic>matrix metallopeptidase 2</italic>
 (<italic>Mmp2</italic>
), and <italic>platelet-derived growth factor-B</italic>
 (<italic>Pdgfb</italic>
), were significantly decreased in B16 tumors grown in <italic>Foxc2</italic>
+/- mice, and tumor blood vessels formed in <italic>Foxc2</italic>
+/- mice showed reduced coverage of mural cells and endothelial cell apoptosis. In addition, the tumor tissue in <italic>Foxc2</italic>
+/- mice had an accumulation of necrotic cells. Taken together, these findings demonstrate that haplodeficiency of <italic>Foxc2</italic>
 results in impaired formation of tumor blood vessels as well as reduced tumor growth and thereby provide evidence that Foxc2 is critical for tumor development and angiogenesis.</p>
</div>
</front>
</TEI>
<pmc article-type="research-article" xml:lang="EN"><pmc-comment>The publisher of this article does not allow downloading of the full text in XML form.</pmc-comment>
  <pmc-dir>properties manuscript</pmc-dir>
  <front><journal-meta><journal-id journal-id-type="nlm-journal-id">0372516</journal-id>
<journal-id journal-id-type="pubmed-jr-id">1008</journal-id>
<journal-id journal-id-type="nlm-ta">Biochem Biophys Res Commun</journal-id>
<journal-title>Biochemical and biophysical research communications</journal-title>
<issn pub-type="ppub">0006-291X</issn>
<issn pub-type="epub">1090-2104</issn>
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<article-meta><article-id pub-id-type="pmid">20060810</article-id>
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<article-id pub-id-type="doi">10.1016/j.bbrc.2010.01.015</article-id>
<article-id pub-id-type="manuscript">NIHMS169896</article-id>
<article-categories><subj-group subj-group-type="heading"><subject>Article</subject>
</subj-group>
</article-categories>
<title-group><article-title>The Foxc2 transcription factor regulates tumor angiogenesis</article-title>
</title-group>
<contrib-group><contrib contrib-type="author"><name><surname>Sano</surname>
<given-names>Hideto</given-names>
</name>
<xref rid="A1" ref-type="aff">a</xref>
</contrib>
<contrib contrib-type="author"><name><surname>LeBoeuf</surname>
<given-names>Jared P</given-names>
</name>
<xref rid="A1" ref-type="aff">a</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Novitsky</surname>
<given-names>Sergey V</given-names>
</name>
<xref rid="A2" ref-type="aff">b</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Seo</surname>
<given-names>Seungwoon</given-names>
</name>
<xref rid="A1" ref-type="aff">a</xref>
<xref rid="FN2" ref-type="author-notes">1</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Zaja-Milatovic</surname>
<given-names>Snjezana</given-names>
</name>
<xref rid="A2" ref-type="aff">b</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Dikov</surname>
<given-names>Mikhail M.</given-names>
</name>
<xref rid="A2" ref-type="aff">b</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Kume</surname>
<given-names>Tsutomu</given-names>
</name>
<xref rid="A1" ref-type="aff">a</xref>
<xref rid="FN2" ref-type="author-notes">1</xref>
</contrib>
</contrib-group>
<aff id="A1"><label>a</label>
Division of Cardiovascular Medicine, Department of Medicine, Vanderbilt University Medical Center, 2220 Pierce Ave, Nashville, TN 37232-6300, USA</aff>
<aff id="A2"><label>b</label>
Hematology Oncology, Department of Medicine, Vanderbilt University Medical Center, 2220 Pierce Ave, Nashville, TN 37232-6300, USA</aff>
<author-notes><corresp id="FN1">Address correspondence to: Tsutomu Kume, Feinberg Cardiovascular Research Institute, Northwestern University School of Medicine, Tarry 14-731, 303 E Chicago Ave, Chicago, IL 60611, USA, Fax: 1-312-503-0137, <email>t-kume@northwestern.edu</email>
</corresp>
<fn id="FN2" fn-type="present-address"><label>1</label>
<p>Present address: Feinberg Cardiovascular Research Institute, Northwestern University School of Medicine</p>
</fn>
</author-notes>
<pub-date pub-type="nihms-submitted"><day>26</day>
<month>1</month>
<year>2010</year>
</pub-date>
<pub-date pub-type="epub"><day>12</day>
<month>1</month>
<year>2010</year>
</pub-date>
<pub-date pub-type="ppub"><day>5</day>
<month>2</month>
<year>2010</year>
</pub-date>
<pub-date pub-type="pmc-release"><day>5</day>
<month>2</month>
<year>2011</year>
</pub-date>
<volume>392</volume>
<issue>2</issue>
<fpage>201</fpage>
<abstract><p id="P1">The Forkhead/Fox transcription factor Foxc2 is a critical regulator of vascular development. However, the role of Foxc2 in pathological angiogenesis in cancer remains unknown. Here we show that FoxC2 is highly expressed in human breast and colonic tumors and in the tumor endothelium in human and mouse melanomas. Using the B16 melanoma tumor model, we investigated the function of Foxc2 in tumor angiogenesis. After subcutaneous injection of B16 melanoma cells, primary tumor growth as well as neovascularization was markedly reduced in mice lacking one copy of the <italic>Foxc2</italic>
 gene (<italic>Foxc2</italic>
+/-). Consistently, expression levels of several angiogenic factors, including <italic>vascular endothelial growth factor</italic>
 (<italic>Vegf</italic>
), <italic>matrix metallopeptidase 2</italic>
 (<italic>Mmp2</italic>
), and <italic>platelet-derived growth factor-B</italic>
 (<italic>Pdgfb</italic>
), were significantly decreased in B16 tumors grown in <italic>Foxc2</italic>
+/- mice, and tumor blood vessels formed in <italic>Foxc2</italic>
+/- mice showed reduced coverage of mural cells and endothelial cell apoptosis. In addition, the tumor tissue in <italic>Foxc2</italic>
+/- mice had an accumulation of necrotic cells. Taken together, these findings demonstrate that haplodeficiency of <italic>Foxc2</italic>
 results in impaired formation of tumor blood vessels as well as reduced tumor growth and thereby provide evidence that Foxc2 is critical for tumor development and angiogenesis.</p>
</abstract>
<kwd-group><kwd>Tumor angiogenesis</kwd>
<kwd>VEGF</kwd>
<kwd>Dll4</kwd>
<kwd>PDGF</kwd>
<kwd>Forkhead</kwd>
<kwd>endothelial cell</kwd>
</kwd-group>
<contract-num rid="HL1">R01 HL074121-04
				||HL</contract-num>
<contract-num rid="HL1">R01 HL074121-03
				||HL</contract-num>
<contract-num rid="HL1">R01 HL074121-02
				||HL</contract-num>
<contract-sponsor id="HL1">National Heart, Lung, and Blood Institute : NHLBI</contract-sponsor>
</article-meta>
</front>
</pmc>
</record>

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The Foxc2 transcription factor regulates tumor angiogenesis

The Foxc2 transcription factor regulates tumor angiogenesis

Source :

Abstract

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