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Depletion of β-Arrestin-2 Promotes Tumor Growth and Angiogenesis in a Murine Model of Lung Cancer
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| Zeitschriftentitel: | The Journal of Immunology |
|---|---|
| Personen und Körperschaften: | , , , , |
| In: | The Journal of Immunology, 180, 2008, 8, S. 5699-5706 |
| Format: | E-Article |
| Sprache: | Englisch |
| veröffentlicht: |
The American Association of Immunologists
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| Schlagwörter: |
| author_facet |
Raghuwanshi, Sandeep K. Nasser, Mohd W. Chen, Xiaoxin Strieter, Robert M. Richardson, Ricardo M. Raghuwanshi, Sandeep K. Nasser, Mohd W. Chen, Xiaoxin Strieter, Robert M. Richardson, Ricardo M. |
|---|---|
| author |
Raghuwanshi, Sandeep K. Nasser, Mohd W. Chen, Xiaoxin Strieter, Robert M. Richardson, Ricardo M. |
| spellingShingle |
Raghuwanshi, Sandeep K. Nasser, Mohd W. Chen, Xiaoxin Strieter, Robert M. Richardson, Ricardo M. The Journal of Immunology Depletion of β-Arrestin-2 Promotes Tumor Growth and Angiogenesis in a Murine Model of Lung Cancer Immunology Immunology and Allergy |
| author_sort |
raghuwanshi, sandeep k. |
| spelling |
Raghuwanshi, Sandeep K. Nasser, Mohd W. Chen, Xiaoxin Strieter, Robert M. Richardson, Ricardo M. 0022-1767 1550-6606 The American Association of Immunologists Immunology Immunology and Allergy http://dx.doi.org/10.4049/jimmunol.180.8.5699 <jats:title>Abstract</jats:title> <jats:p>Arrestins are adaptor/scaffold proteins that complex with activated and phosphorylated G protein-coupled receptor to terminate G protein activation and signal transduction. These complexes also mediate downstream signaling, independently of G protein activation. We have previously shown that β-arrestin-2 (βarr2) depletion promotes CXCR2-mediated cellular signaling, including angiogenesis and excisional wound closure. This study was designed to investigate the role of βarr2 in tumorigenesis using a murine model of lung cancer. To that end, heterotopic murine Lewis lung cancer and tail vein metastasis tumor model systems in βarr2-deficient mice (βarr2−/−) and control littermates (βarr2+/+) were used. βarr2−/− mice exhibited a significant increase in Lewis lung cancer tumor growth and metastasis relative to βarr2+/+ mice. This correlated with decreased number of tumor-infiltrating lymphocytes but with elevated levels of the ELR+ chemokines (CXCL1/keratinocyte-derived chemokine and CXCL2/MIP-2), vascular endothelial growth factor, and microvessel density. NF-κB activity was also enhanced in βarr2−/− mice, whereas hypoxia-inducible factor-1α expression was decreased. Inhibition of CXCR2 or NF-κB reduced tumor growth in both βarr2−/− and βarr2+/+ mice. NF-κB inhibition also decreased ELR+ chemokines and vascular endothelial growth factor expression. Altogether, the data suggest that βarr2 modulates tumorigenesis by regulating inflammation and angiogenesis through activation of CXCR2 and NF-κB.</jats:p> Depletion of β-Arrestin-2 Promotes Tumor Growth and Angiogenesis in a Murine Model of Lung Cancer The Journal of Immunology |
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The American Association of Immunologists, 2008 |
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The American Association of Immunologists, 2008 |
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| title |
Depletion of β-Arrestin-2 Promotes Tumor Growth and Angiogenesis in a Murine Model of Lung Cancer |
| title_unstemmed |
Depletion of β-Arrestin-2 Promotes Tumor Growth and Angiogenesis in a Murine Model of Lung Cancer |
| title_full |
Depletion of β-Arrestin-2 Promotes Tumor Growth and Angiogenesis in a Murine Model of Lung Cancer |
| title_fullStr |
Depletion of β-Arrestin-2 Promotes Tumor Growth and Angiogenesis in a Murine Model of Lung Cancer |
| title_full_unstemmed |
Depletion of β-Arrestin-2 Promotes Tumor Growth and Angiogenesis in a Murine Model of Lung Cancer |
| title_short |
Depletion of β-Arrestin-2 Promotes Tumor Growth and Angiogenesis in a Murine Model of Lung Cancer |
| title_sort |
depletion of β-arrestin-2 promotes tumor growth and angiogenesis in a murine model of lung cancer |
| topic |
Immunology Immunology and Allergy |
| url |
http://dx.doi.org/10.4049/jimmunol.180.8.5699 |
| publishDate |
2008 |
| physical |
5699-5706 |
| description |
<jats:title>Abstract</jats:title>
<jats:p>Arrestins are adaptor/scaffold proteins that complex with activated and phosphorylated G protein-coupled receptor to terminate G protein activation and signal transduction. These complexes also mediate downstream signaling, independently of G protein activation. We have previously shown that β-arrestin-2 (βarr2) depletion promotes CXCR2-mediated cellular signaling, including angiogenesis and excisional wound closure. This study was designed to investigate the role of βarr2 in tumorigenesis using a murine model of lung cancer. To that end, heterotopic murine Lewis lung cancer and tail vein metastasis tumor model systems in βarr2-deficient mice (βarr2−/−) and control littermates (βarr2+/+) were used. βarr2−/− mice exhibited a significant increase in Lewis lung cancer tumor growth and metastasis relative to βarr2+/+ mice. This correlated with decreased number of tumor-infiltrating lymphocytes but with elevated levels of the ELR+ chemokines (CXCL1/keratinocyte-derived chemokine and CXCL2/MIP-2), vascular endothelial growth factor, and microvessel density. NF-κB activity was also enhanced in βarr2−/− mice, whereas hypoxia-inducible factor-1α expression was decreased. Inhibition of CXCR2 or NF-κB reduced tumor growth in both βarr2−/− and βarr2+/+ mice. NF-κB inhibition also decreased ELR+ chemokines and vascular endothelial growth factor expression. Altogether, the data suggest that βarr2 modulates tumorigenesis by regulating inflammation and angiogenesis through activation of CXCR2 and NF-κB.</jats:p> |
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| author | Raghuwanshi, Sandeep K., Nasser, Mohd W., Chen, Xiaoxin, Strieter, Robert M., Richardson, Ricardo M. |
| author_facet | Raghuwanshi, Sandeep K., Nasser, Mohd W., Chen, Xiaoxin, Strieter, Robert M., Richardson, Ricardo M., Raghuwanshi, Sandeep K., Nasser, Mohd W., Chen, Xiaoxin, Strieter, Robert M., Richardson, Ricardo M. |
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| description | <jats:title>Abstract</jats:title> <jats:p>Arrestins are adaptor/scaffold proteins that complex with activated and phosphorylated G protein-coupled receptor to terminate G protein activation and signal transduction. These complexes also mediate downstream signaling, independently of G protein activation. We have previously shown that β-arrestin-2 (βarr2) depletion promotes CXCR2-mediated cellular signaling, including angiogenesis and excisional wound closure. This study was designed to investigate the role of βarr2 in tumorigenesis using a murine model of lung cancer. To that end, heterotopic murine Lewis lung cancer and tail vein metastasis tumor model systems in βarr2-deficient mice (βarr2−/−) and control littermates (βarr2+/+) were used. βarr2−/− mice exhibited a significant increase in Lewis lung cancer tumor growth and metastasis relative to βarr2+/+ mice. This correlated with decreased number of tumor-infiltrating lymphocytes but with elevated levels of the ELR+ chemokines (CXCL1/keratinocyte-derived chemokine and CXCL2/MIP-2), vascular endothelial growth factor, and microvessel density. NF-κB activity was also enhanced in βarr2−/− mice, whereas hypoxia-inducible factor-1α expression was decreased. Inhibition of CXCR2 or NF-κB reduced tumor growth in both βarr2−/− and βarr2+/+ mice. NF-κB inhibition also decreased ELR+ chemokines and vascular endothelial growth factor expression. Altogether, the data suggest that βarr2 modulates tumorigenesis by regulating inflammation and angiogenesis through activation of CXCR2 and NF-κB.</jats:p> |
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| spelling | Raghuwanshi, Sandeep K. Nasser, Mohd W. Chen, Xiaoxin Strieter, Robert M. Richardson, Ricardo M. 0022-1767 1550-6606 The American Association of Immunologists Immunology Immunology and Allergy http://dx.doi.org/10.4049/jimmunol.180.8.5699 <jats:title>Abstract</jats:title> <jats:p>Arrestins are adaptor/scaffold proteins that complex with activated and phosphorylated G protein-coupled receptor to terminate G protein activation and signal transduction. These complexes also mediate downstream signaling, independently of G protein activation. We have previously shown that β-arrestin-2 (βarr2) depletion promotes CXCR2-mediated cellular signaling, including angiogenesis and excisional wound closure. This study was designed to investigate the role of βarr2 in tumorigenesis using a murine model of lung cancer. To that end, heterotopic murine Lewis lung cancer and tail vein metastasis tumor model systems in βarr2-deficient mice (βarr2−/−) and control littermates (βarr2+/+) were used. βarr2−/− mice exhibited a significant increase in Lewis lung cancer tumor growth and metastasis relative to βarr2+/+ mice. This correlated with decreased number of tumor-infiltrating lymphocytes but with elevated levels of the ELR+ chemokines (CXCL1/keratinocyte-derived chemokine and CXCL2/MIP-2), vascular endothelial growth factor, and microvessel density. NF-κB activity was also enhanced in βarr2−/− mice, whereas hypoxia-inducible factor-1α expression was decreased. Inhibition of CXCR2 or NF-κB reduced tumor growth in both βarr2−/− and βarr2+/+ mice. NF-κB inhibition also decreased ELR+ chemokines and vascular endothelial growth factor expression. Altogether, the data suggest that βarr2 modulates tumorigenesis by regulating inflammation and angiogenesis through activation of CXCR2 and NF-κB.</jats:p> Depletion of β-Arrestin-2 Promotes Tumor Growth and Angiogenesis in a Murine Model of Lung Cancer The Journal of Immunology |
| spellingShingle | Raghuwanshi, Sandeep K., Nasser, Mohd W., Chen, Xiaoxin, Strieter, Robert M., Richardson, Ricardo M., The Journal of Immunology, Depletion of β-Arrestin-2 Promotes Tumor Growth and Angiogenesis in a Murine Model of Lung Cancer, Immunology, Immunology and Allergy |
| title | Depletion of β-Arrestin-2 Promotes Tumor Growth and Angiogenesis in a Murine Model of Lung Cancer |
| title_full | Depletion of β-Arrestin-2 Promotes Tumor Growth and Angiogenesis in a Murine Model of Lung Cancer |
| title_fullStr | Depletion of β-Arrestin-2 Promotes Tumor Growth and Angiogenesis in a Murine Model of Lung Cancer |
| title_full_unstemmed | Depletion of β-Arrestin-2 Promotes Tumor Growth and Angiogenesis in a Murine Model of Lung Cancer |
| title_short | Depletion of β-Arrestin-2 Promotes Tumor Growth and Angiogenesis in a Murine Model of Lung Cancer |
| title_sort | depletion of β-arrestin-2 promotes tumor growth and angiogenesis in a murine model of lung cancer |
| title_unstemmed | Depletion of β-Arrestin-2 Promotes Tumor Growth and Angiogenesis in a Murine Model of Lung Cancer |
| topic | Immunology, Immunology and Allergy |
| url | http://dx.doi.org/10.4049/jimmunol.180.8.5699 |