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Adrenomedullin gene dosage correlates with tumor and lymph node lymphangiogenesis

Identifieur interne : 005249 ( Ncbi/Merge ); précédent : 005248; suivant : 005250

Adrenomedullin gene dosage correlates with tumor and lymph node lymphangiogenesis

Auteurs : Natalie O. Karpinich ; Daniel O. Kechele ; Scott T. Espenschied ; Helen H. Willcockson ; Yuri Fedoriw ; Kathleen M. Caron [États-Unis]

Source :

RBID : PMC:3545524

Abstract

Adrenomedullin (AM) is a potent lymphangiogenic factor that promotes lymphatic endothelial cell (LEC) proliferation through a pharmacologically tractable G-protein-coupled receptor. Numerous types of human cancers have increased levels of AM; however, the functional consequences of this fact have not been characterized. Therefore, we evaluated whether modulating adrenomedullin (Adm) gene dosage within tumor cells affects lymphangiogenesis. Murine Lewis lung carcinoma (LLC) cells that overexpress or underexpress Adm were injected subcutaneously into C57BL/6 mice, and tumors were evaluated for growth and vascularization. A dosage range from ∼10 to 200% of wild-type Adm expression did not affect LLC proliferation in vitro or in vivo, nor did it affect angiogenesis. Notably, the dosage of Adm markedly and significantly influenced tumor lymphangiogenesis. Reduced Adm expression in tumors decreased the proliferation of LECs and the number of lymphatic vessels, while elevated tumor Adm expression led to enlarged lymphatic vessels. Moreover, overexpression of Adm in tumors induced sentinel lymph node lymphangiogenesis and led to an increased incidence of Ki67-positive foci within the lung. These data show that tumor-secreted AM is a critical factor for driving both tumor and lymph node lymphangiogenesis. Thus, pharmacological targeting of AM signaling may provide a new avenue for inhibition of tumor lymphangiogenesis.—Karpinich, N. O., Kechele, D. O., Espenschied, S. T., Willcockson, H. H., Fedoriw, Y., Caron, K. M. Adrenomedullin gene dosage correlates with tumor and lymph node lymphangiogenesis.


Url:
DOI: 10.1096/fj.12-214080
PubMed: 23099649
PubMed Central: 3545524

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PMC:3545524

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<p>Adrenomedullin (AM) is a potent lymphangiogenic factor that promotes lymphatic endothelial cell (LEC) proliferation through a pharmacologically tractable G-protein-coupled receptor. Numerous types of human cancers have increased levels of AM; however, the functional consequences of this fact have not been characterized. Therefore, we evaluated whether modulating adrenomedullin (
<italic>Adm</italic>
) gene dosage within tumor cells affects lymphangiogenesis. Murine Lewis lung carcinoma (LLC) cells that overexpress or underexpress
<italic>Adm</italic>
were injected subcutaneously into C57BL/6 mice, and tumors were evaluated for growth and vascularization. A dosage range from ∼10 to 200% of wild-type
<italic>Adm</italic>
expression did not affect LLC proliferation
<italic>in vitro</italic>
or
<italic>in vivo</italic>
, nor did it affect angiogenesis. Notably, the dosage of
<italic>Adm</italic>
markedly and significantly influenced tumor lymphangiogenesis. Reduced
<italic>Adm</italic>
expression in tumors decreased the proliferation of LECs and the number of lymphatic vessels, while elevated tumor
<italic>Adm</italic>
expression led to enlarged lymphatic vessels. Moreover, overexpression of
<italic>Adm</italic>
in tumors induced sentinel lymph node lymphangiogenesis and led to an increased incidence of Ki67-positive foci within the lung. These data show that tumor-secreted AM is a critical factor for driving both tumor and lymph node lymphangiogenesis. Thus, pharmacological targeting of AM signaling may provide a new avenue for inhibition of tumor lymphangiogenesis.—Karpinich, N. O., Kechele, D. O., Espenschied, S. T., Willcockson, H. H., Fedoriw, Y., Caron, K. M. Adrenomedullin gene dosage correlates with tumor and lymph node lymphangiogenesis.</p>
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<article-title>Adrenomedullin gene dosage correlates with tumor and lymph node lymphangiogenesis</article-title>
</title-group>
<contrib-group>
<contrib contrib-type="author">
<name>
<surname>Karpinich</surname>
<given-names>Natalie O.</given-names>
</name>
<xref ref-type="aff" rid="aff1">*</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Kechele</surname>
<given-names>Daniel O.</given-names>
</name>
<xref ref-type="aff" rid="aff1">*</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Espenschied</surname>
<given-names>Scott T.</given-names>
</name>
<xref ref-type="aff" rid="aff1">*</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Willcockson</surname>
<given-names>Helen H.</given-names>
</name>
<xref ref-type="aff" rid="aff1">*</xref>
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<contrib contrib-type="author">
<name>
<surname>Fedoriw</surname>
<given-names>Yuri</given-names>
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<sup>†</sup>
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</contrib>
<contrib contrib-type="author">
<name>
<surname>Caron</surname>
<given-names>Kathleen M.</given-names>
</name>
<xref ref-type="aff" rid="aff1">*</xref>
<xref ref-type="aff" rid="aff3">
<sup>‡</sup>
</xref>
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<sup>1</sup>
</xref>
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<aff id="aff1">
<label>*</label>
Department of Cell and Molecular Physiology,</aff>
<aff id="aff2">
<label>†</label>
Department of Pathology and Laboratory Medicine, and</aff>
<aff id="aff3">
<label>‡</label>
Department of Genetics, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA</aff>
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<label>1</label>
<addr-line>Department of Cell and Molecular Physiology, University of North Carolina at Chapel Hill, 111 Mason Farm Rd., CB 7545, 6330 MBRB, Chapel Hill, NC 27599 USA</addr-line>
. E-mail:
<email>kathleen_caron@med.unc.edu</email>
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<month>2</month>
<year>2014</year>
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<volume>27</volume>
<issue>2</issue>
<fpage>590</fpage>
<lpage>600</lpage>
<history>
<date date-type="received">
<day>8</day>
<month>6</month>
<year>2012</year>
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<date date-type="accepted">
<day>15</day>
<month>10</month>
<year>2012</year>
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<copyright-year>2013</copyright-year>
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<self-uri xlink:title="pdf" xlink:type="simple" xlink:href="z3800213000590.pdf"></self-uri>
<abstract>
<p>Adrenomedullin (AM) is a potent lymphangiogenic factor that promotes lymphatic endothelial cell (LEC) proliferation through a pharmacologically tractable G-protein-coupled receptor. Numerous types of human cancers have increased levels of AM; however, the functional consequences of this fact have not been characterized. Therefore, we evaluated whether modulating adrenomedullin (
<italic>Adm</italic>
) gene dosage within tumor cells affects lymphangiogenesis. Murine Lewis lung carcinoma (LLC) cells that overexpress or underexpress
<italic>Adm</italic>
were injected subcutaneously into C57BL/6 mice, and tumors were evaluated for growth and vascularization. A dosage range from ∼10 to 200% of wild-type
<italic>Adm</italic>
expression did not affect LLC proliferation
<italic>in vitro</italic>
or
<italic>in vivo</italic>
, nor did it affect angiogenesis. Notably, the dosage of
<italic>Adm</italic>
markedly and significantly influenced tumor lymphangiogenesis. Reduced
<italic>Adm</italic>
expression in tumors decreased the proliferation of LECs and the number of lymphatic vessels, while elevated tumor
<italic>Adm</italic>
expression led to enlarged lymphatic vessels. Moreover, overexpression of
<italic>Adm</italic>
in tumors induced sentinel lymph node lymphangiogenesis and led to an increased incidence of Ki67-positive foci within the lung. These data show that tumor-secreted AM is a critical factor for driving both tumor and lymph node lymphangiogenesis. Thus, pharmacological targeting of AM signaling may provide a new avenue for inhibition of tumor lymphangiogenesis.—Karpinich, N. O., Kechele, D. O., Espenschied, S. T., Willcockson, H. H., Fedoriw, Y., Caron, K. M. Adrenomedullin gene dosage correlates with tumor and lymph node lymphangiogenesis.</p>
</abstract>
<kwd-group>
<kwd>cancer</kwd>
<kwd>endothelial cells</kwd>
<kwd>metastasis</kwd>
<kwd>mouse models</kwd>
</kwd-group>
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</front>
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<name sortKey="Espenschied, Scott T" sort="Espenschied, Scott T" uniqKey="Espenschied S" first="Scott T." last="Espenschied">Scott T. Espenschied</name>
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<region name="Caroline du Nord">
<name sortKey="Caron, Kathleen M" sort="Caron, Kathleen M" uniqKey="Caron K" first="Kathleen M." last="Caron">Kathleen M. Caron</name>
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