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Egfl7 Promotes Tumor Escape from Immunity by Repressing Endothelial Cell Activation

Downregulating the leukocyte adhesion molecules expressed by endothelial cells that line tumor blood vessels can limit the entry of immune effector cells into the tumor mass, thereby contributing to tumoral immune escape. Egfl7 (also known as VE-statin) is a secreted protein specifically expressed b...

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Published in:Cancer research (Chicago, Ill.) Ill.), 2011-12, Vol.71 (23), p.7176-7186
Main Authors: DELFORTRIE, Suzanne, PINTE, Sébastien, FAVEEUW, Christelle, SONCIN, Fabrice, MATTOT, Virginie, SAMSON, Chantal, VILLAIN, Gaëlle, CAETANO, Bertrand, LAURIDANT-PHILIPPIN, Géraldine, BARANZELLI, Marie-Christine, BONNETERRE, Jacques, TROTTEIN, François
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cited_by cdi_FETCH-LOGICAL-c587t-33302249fa63a0c54292a6ea0dc54be670f390403da57d8a98c01cd07045abc43
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container_title Cancer research (Chicago, Ill.)
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creator DELFORTRIE, Suzanne
PINTE, Sébastien
FAVEEUW, Christelle
SONCIN, Fabrice
MATTOT, Virginie
SAMSON, Chantal
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CAETANO, Bertrand
LAURIDANT-PHILIPPIN, Géraldine
BARANZELLI, Marie-Christine
BONNETERRE, Jacques
TROTTEIN, François
description Downregulating the leukocyte adhesion molecules expressed by endothelial cells that line tumor blood vessels can limit the entry of immune effector cells into the tumor mass, thereby contributing to tumoral immune escape. Egfl7 (also known as VE-statin) is a secreted protein specifically expressed by endothelial cells in normal tissues and by cancer cells in various human tumors. High levels of Egfl7 correlate with higher tumor grade and poorer prognosis. Here we show that expression of Egfl7 in breast and lung carcinoma cells accelerates tumor growth and metastasis in immunocompetent mice but not in immunodeficient mice. Tumors expressing Egfl7 were infiltrated relatively poorly by immune cells and were characterized by reduced levels of immunostimulatory cytokines [IFN-γ, interleukin-12 (IL-12)] and fewer endothelial adhesion molecules [intercellular adhesion molecule 1 (ICAM-1) and vascular cell adhesion molecule 1 (VCAM-1)]. In vitro studies revealed that Egfl7 inhibited the expression of leukocyte adhesion molecules by endothelial cells, preventing lymphocyte adhesion. In contrast, Egfl7 did not exert any effects on immune cell activation. Human breast cancer lesions expressing high levels of Egfl7 also expressed less ICAM-1 and VCAM-1 in their blood vessels, also indicating an inverse correlation between expression levels of Egfl7 and IFN-γ. Thus, Egfl7 expression in tumors promotes tumor progression by reducing the expression of endothelial molecules that mediate immune cell infiltration. Our findings highlight a novel mechanism through which tumors escape immune control.
doi_str_mv 10.1158/0008-5472.can-11-1301
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Egfl7 (also known as VE-statin) is a secreted protein specifically expressed by endothelial cells in normal tissues and by cancer cells in various human tumors. High levels of Egfl7 correlate with higher tumor grade and poorer prognosis. Here we show that expression of Egfl7 in breast and lung carcinoma cells accelerates tumor growth and metastasis in immunocompetent mice but not in immunodeficient mice. Tumors expressing Egfl7 were infiltrated relatively poorly by immune cells and were characterized by reduced levels of immunostimulatory cytokines [IFN-γ, interleukin-12 (IL-12)] and fewer endothelial adhesion molecules [intercellular adhesion molecule 1 (ICAM-1) and vascular cell adhesion molecule 1 (VCAM-1)]. In vitro studies revealed that Egfl7 inhibited the expression of leukocyte adhesion molecules by endothelial cells, preventing lymphocyte adhesion. In contrast, Egfl7 did not exert any effects on immune cell activation. Human breast cancer lesions expressing high levels of Egfl7 also expressed less ICAM-1 and VCAM-1 in their blood vessels, also indicating an inverse correlation between expression levels of Egfl7 and IFN-γ. Thus, Egfl7 expression in tumors promotes tumor progression by reducing the expression of endothelial molecules that mediate immune cell infiltration. 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Human breast cancer lesions expressing high levels of Egfl7 also expressed less ICAM-1 and VCAM-1 in their blood vessels, also indicating an inverse correlation between expression levels of Egfl7 and IFN-γ. Thus, Egfl7 expression in tumors promotes tumor progression by reducing the expression of endothelial molecules that mediate immune cell infiltration. 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Human breast cancer lesions expressing high levels of Egfl7 also expressed less ICAM-1 and VCAM-1 in their blood vessels, also indicating an inverse correlation between expression levels of Egfl7 and IFN-γ. Thus, Egfl7 expression in tumors promotes tumor progression by reducing the expression of endothelial molecules that mediate immune cell infiltration. Our findings highlight a novel mechanism through which tumors escape immune control.</abstract><cop>Philadelphia, PA</cop><pub>American Association for Cancer Research</pub><pmid>22037871</pmid><doi>10.1158/0008-5472.can-11-1301</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record>
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subjects Animals
Antineoplastic agents
Biological and medical sciences
Cell Adhesion - genetics
Cell Adhesion - immunology
Cell Adhesion Molecules - genetics
Cell Adhesion Molecules - immunology
Cell Line, Tumor
Cell Transformation, Neoplastic - genetics
Cell Transformation, Neoplastic - immunology
Cell Transformation, Neoplastic - metabolism
Cell Transformation, Neoplastic - pathology
Cells, Cultured
Disease Progression
Endothelial Cells - immunology
Endothelial Cells - pathology
Endothelial Growth Factors - genetics
Endothelial Growth Factors - immunology
Endothelium, Vascular - immunology
Endothelium, Vascular - pathology
Female
Human Umbilical Vein Endothelial Cells
Humans
Intercellular Adhesion Molecule-1 - genetics
Intercellular Adhesion Molecule-1 - immunology
Interferon-gamma - genetics
Interferon-gamma - immunology
Interferon-gamma - metabolism
Interleukin-12 - genetics
Interleukin-12 - immunology
Interleukin-12 - metabolism
Jurkat Cells
Medical sciences
Mice
Mice, Inbred BALB C
Mice, Inbred C57BL
Mice, SCID
Neoplasm Metastasis - genetics
Neoplasm Metastasis - immunology
Neoplasm Metastasis - pathology
Pharmacology. Drug treatments
Proteins - genetics
Proteins - immunology
Tumor Escape - genetics
Tumor Escape - immunology
Tumors
Vascular Cell Adhesion Molecule-1 - genetics
Vascular Cell Adhesion Molecule-1 - immunology
title Egfl7 Promotes Tumor Escape from Immunity by Repressing Endothelial Cell Activation
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