ADAM8 expression in invasive breast cancer promotes tumor dissemination and metastasis
The transmembrane metalloprotease‐disintegrin ADAM8 mediates cell adhesion and shedding of ligands, receptors and extracellular matrix components. Here, we report that ADAM8 is abundantly expressed in breast tumors and derived metastases compared to normal tissue, especially in triple‐negative breas...
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| Vydáno v: | EMBO molecular medicine Ročník 6; číslo 2; s. 278 - 294 |
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| Hlavní autoři: | , , , , , , , , , , , , , , , |
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| Jazyk: | angličtina |
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Nature Publishing Group UK
01.02.2014
Wiley Open Access Blackwell Publishing Ltd Springer Nature |
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| ISSN: | 1757-4676, 1757-4684, 1757-4684 |
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| Abstract | The transmembrane metalloprotease‐disintegrin ADAM8 mediates cell adhesion and shedding of ligands, receptors and extracellular matrix components. Here, we report that ADAM8 is abundantly expressed in breast tumors and derived metastases compared to normal tissue, especially in triple‐negative breast cancers (TNBCs). Furthermore, high
ADAM8
levels predicted poor patient outcome. Consistently, ADAM8 promoted an aggressive phenotype of TNBC cells in culture. In a mouse orthotopic model, tumors derived from TNBC cells with ADAM8 knockdown failed to grow beyond a palpable size and displayed poor vascularization. Circulating tumor cells and brain metastases were also significantly reduced. Mechanistically, ADAM8 stimulated both angiogenesis through release of VEGF‐A and transendothelial cell migration via β1‐integrin activation.
In vivo
, treatment with an anti‐ADAM8 antibody from the time of cell inoculation reduced primary tumor burden and metastases. Furthermore, antibody treatment of established tumors profoundly decreased metastases in a resection model. As a non‐essential protein under physiological conditions, ADAM8 represents a promising novel target for treatment of TNBCs, which currently lack targeted therapies and frequently progress with fatal dissemination.
Synopsis
The transmembrane protein ADAM8 is shown to be a crucial player in multiple steps of breast tumorigenesis, notably in angiogenesis and cancer cell adhesion to the endothelium. The results validate ADAM8 as novel target for the treatment of aggressive triple‐negative breast cancer
The transmembrane ADAM8 protein is expressed in primary human breast tumors compared to normal breast tissue, and especially in triple‐negative breast cancers (TNBC), which currently have no targeted therapies.
High levels of ADAM8 expression predict poor breast cancer clinical outcome and are detected in half of patient metastases.
ADAM8 promotes tumor growth and dissemination in an orthotopic mouse model by stimulating angiogenesis (via the release of VEGF‐A and other pro‐angiogenic growth factors) and tumor cell intra/extravasation (via activation of β1‐integrin).
Treatment of mice with a monoclonal antibody targeting ADAM8 extracellular domains initiated at the time of TNBC cell implantation in the mammary fat pad significantly reduces tumor growth, angiogenesis and metastasis.
Treatment of pre‐existing tumors with the ADAM8 antibody in a neoadjuvant setting profoundly reduces metastases in a mouse resection model, further validating ADAM8 as a therapeutic target of TNBC.
Graphical Abstract
The transmembrane protein ADAM8 is shown to be a crucial player in multiple steps of breast tumorigenesis, notably in angiogenesis and cancer cell adhesion to the endothelium. The results validate ADAM8 as novel target for the treatment of aggressive triple‐negative breast cancer. |
|---|---|
| AbstractList | Abstract The transmembrane metalloprotease‐disintegrin ADAM8 mediates cell adhesion and shedding of ligands, receptors and extracellular matrix components. Here, we report that ADAM8 is abundantly expressed in breast tumors and derived metastases compared to normal tissue, especially in triple‐negative breast cancers (TNBCs). Furthermore, high ADAM8 levels predicted poor patient outcome. Consistently, ADAM8 promoted an aggressive phenotype of TNBC cells in culture. In a mouse orthotopic model, tumors derived from TNBC cells with ADAM8 knockdown failed to grow beyond a palpable size and displayed poor vascularization. Circulating tumor cells and brain metastases were also significantly reduced. Mechanistically, ADAM8 stimulated both angiogenesis through release of VEGF‐A and transendothelial cell migration via β1‐integrin activation. In vivo, treatment with an anti‐ADAM8 antibody from the time of cell inoculation reduced primary tumor burden and metastases. Furthermore, antibody treatment of established tumors profoundly decreased metastases in a resection model. As a non‐essential protein under physiological conditions, ADAM8 represents a promising novel target for treatment of TNBCs, which currently lack targeted therapies and frequently progress with fatal dissemination. The transmembrane metalloprotease‐disintegrin ADAM8 mediates cell adhesion and shedding of ligands, receptors and extracellular matrix components. Here, we report that ADAM8 is abundantly expressed in breast tumors and derived metastases compared to normal tissue, especially in triple‐negative breast cancers (TNBCs). Furthermore, high ADAM8 levels predicted poor patient outcome. Consistently, ADAM8 promoted an aggressive phenotype of TNBC cells in culture. In a mouse orthotopic model, tumors derived from TNBC cells with ADAM8 knockdown failed to grow beyond a palpable size and displayed poor vascularization. Circulating tumor cells and brain metastases were also significantly reduced. Mechanistically, ADAM8 stimulated both angiogenesis through release of VEGF‐A and transendothelial cell migration via β1‐integrin activation. In vivo, treatment with an anti‐ADAM8 antibody from the time of cell inoculation reduced primary tumor burden and metastases. Furthermore, antibody treatment of established tumors profoundly decreased metastases in a resection model. As a non‐essential protein under physiological conditions, ADAM8 represents a promising novel target for treatment of TNBCs, which currently lack targeted therapies and frequently progress with fatal dissemination. Synopsis The transmembrane protein ADAM8 is shown to be a crucial player in multiple steps of breast tumorigenesis, notably in angiogenesis and cancer cell adhesion to the endothelium. The results validate ADAM8 as novel target for the treatment of aggressive triple‐negative breast cancer The transmembrane ADAM8 protein is expressed in primary human breast tumors compared to normal breast tissue, and especially in triple‐negative breast cancers (TNBC), which currently have no targeted therapies. High levels of ADAM8 expression predict poor breast cancer clinical outcome and are detected in half of patient metastases. ADAM8 promotes tumor growth and dissemination in an orthotopic mouse model by stimulating angiogenesis (via the release of VEGF‐A and other pro‐angiogenic growth factors) and tumor cell intra/extravasation (via activation of β1‐integrin). Treatment of mice with a monoclonal antibody targeting ADAM8 extracellular domains initiated at the time of TNBC cell implantation in the mammary fat pad significantly reduces tumor growth, angiogenesis and metastasis. Treatment of pre‐existing tumors with the ADAM8 antibody in a neoadjuvant setting profoundly reduces metastases in a mouse resection model, further validating ADAM8 as a therapeutic target of TNBC. The transmembrane protein ADAM8 is shown to be a crucial player in multiple steps of breast tumorigenesis, notably in angiogenesis and cancer cell adhesion to the endothelium. The results validate ADAM8 as novel target for the treatment of aggressive triple‐negative breast cancer. The transmembrane metalloprotease-disintegrin ADAM8 mediates cell adhesion and shedding of ligands, receptors and extracellular matrix components. Here, we report that ADAM8 is abundantly expressed in breast tumors and derived metastases compared to normal tissue, especially in triple-negative breast cancers (TNBCs). Furthermore, high ADAM8 levels predicted poor patient outcome. Consistently, ADAM8 promoted an aggressive phenotype of TNBC cells in culture. In a mouse orthotopic model, tumors derived from TNBC cells with ADAM8 knockdown failed to grow beyond a palpable size and displayed poor vascularization. Circulating tumor cells and brain metastases were also significantly reduced. Mechanistically, ADAM8 stimulated both angiogenesis through release of VEGF-A and transendothelial cell migration via β1-integrin activation. In vivo, treatment with an anti-ADAM8 antibody from the time of cell inoculation reduced primary tumor burden and metastases. Furthermore, antibody treatment of established tumors profoundly decreased metastases in a resection model. As a non-essential protein under physiological conditions, ADAM8 represents a promising novel target for treatment of TNBCs, which currently lack targeted therapies and frequently progress with fatal dissemination. The transmembrane metalloprotease-disintegrin ADAM8 mediates cell adhesion and shedding of ligands, receptors and extracellular matrix components. Here, we report that ADAM8 is abundantly expressed in breast tumors and derived metastases compared to normal tissue, especially in triple-negative breast cancers (TNBCs). Furthermore, high ADAM8 levels predicted poor patient outcome. Consistently, ADAM8 promoted an aggressive phenotype of TNBC cells in culture. In a mouse orthotopic model, tumors derived from TNBC cells with ADAM8 knockdown failed to grow beyond a palpable size and displayed poor vascularization. Circulating tumor cells and brain metastases were also significantly reduced. Mechanisti-cally, ADAM8 stimulated both angiogenesis through release of VEGF-A and transendothelial cell migration via β1-integrin activation. In vivo, treatment with an anti-ADAM8 antibody from the time of cell inoculation reduced primary tumor burden and metastases. Furthermore, antibody treatment of established tumors profoundly decreased metastases in a resection model. As a non-essential protein under physiological conditions, ADAM8 represents a promising novel target for treatment of TNBCs, which currently lack targeted therapies and frequently progress with fatal dissemination. The transmembrane metalloprotease‐disintegrin ADAM8 mediates cell adhesion and shedding of ligands, receptors and extracellular matrix components. Here, we report that ADAM8 is abundantly expressed in breast tumors and derived metastases compared to normal tissue, especially in triple‐negative breast cancers (TNBCs). Furthermore, high ADAM8 levels predicted poor patient outcome. Consistently, ADAM8 promoted an aggressive phenotype of TNBC cells in culture. In a mouse orthotopic model, tumors derived from TNBC cells with ADAM8 knockdown failed to grow beyond a palpable size and displayed poor vascularization. Circulating tumor cells and brain metastases were also significantly reduced. Mechanistically, ADAM8 stimulated both angiogenesis through release of VEGF‐A and transendothelial cell migration via β1‐integrin activation. In vivo , treatment with an anti‐ADAM8 antibody from the time of cell inoculation reduced primary tumor burden and metastases. Furthermore, antibody treatment of established tumors profoundly decreased metastases in a resection model. As a non‐essential protein under physiological conditions, ADAM8 represents a promising novel target for treatment of TNBCs, which currently lack targeted therapies and frequently progress with fatal dissemination. Synopsis The transmembrane protein ADAM8 is shown to be a crucial player in multiple steps of breast tumorigenesis, notably in angiogenesis and cancer cell adhesion to the endothelium. The results validate ADAM8 as novel target for the treatment of aggressive triple‐negative breast cancer The transmembrane ADAM8 protein is expressed in primary human breast tumors compared to normal breast tissue, and especially in triple‐negative breast cancers (TNBC), which currently have no targeted therapies. High levels of ADAM8 expression predict poor breast cancer clinical outcome and are detected in half of patient metastases. ADAM8 promotes tumor growth and dissemination in an orthotopic mouse model by stimulating angiogenesis (via the release of VEGF‐A and other pro‐angiogenic growth factors) and tumor cell intra/extravasation (via activation of β1‐integrin). Treatment of mice with a monoclonal antibody targeting ADAM8 extracellular domains initiated at the time of TNBC cell implantation in the mammary fat pad significantly reduces tumor growth, angiogenesis and metastasis. Treatment of pre‐existing tumors with the ADAM8 antibody in a neoadjuvant setting profoundly reduces metastases in a mouse resection model, further validating ADAM8 as a therapeutic target of TNBC. Graphical Abstract The transmembrane protein ADAM8 is shown to be a crucial player in multiple steps of breast tumorigenesis, notably in angiogenesis and cancer cell adhesion to the endothelium. The results validate ADAM8 as novel target for the treatment of aggressive triple‐negative breast cancer. The transmembrane metalloprotease-disintegrin ADAM8 mediates cell adhesion and shedding of ligands, receptors and extracellular matrix components. Here, we report that ADAM8 is abundantly expressed in breast tumors and derived metastases compared to normal tissue, especially in triple-negative breast cancers (TNBCs). Furthermore, high ADAM8 levels predicted poor patient outcome. Consistently, ADAM8 promoted an aggressive phenotype of TNBC cells in culture. In a mouse orthotopic model, tumors derived from TNBC cells with ADAM8 knockdown failed to grow beyond a palpable size and displayed poor vascularization. Circulating tumor cells and brain metastases were also significantly reduced. Mechanistically, ADAM8 stimulated both angiogenesis through release of VEGF-A and transendothelial cell migration via β1-integrin activation. In vivo, treatment with an anti-ADAM8 antibody from the time of cell inoculation reduced primary tumor burden and metastases. Furthermore, antibody treatment of established tumors profoundly decreased metastases in a resection model. As a non-essential protein under physiological conditions, ADAM8 represents a promising novel target for treatment of TNBCs, which currently lack targeted therapies and frequently progress with fatal dissemination. Subject Category Cancer The transmembrane metalloprotease-disintegrin ADAM8 mediates cell adhesion and shedding of ligands, receptors and extracellular matrix components. Here, we report that ADAM8 is abundantly expressed in breast tumors and derived metastases compared to normal tissue, especially in triple-negative breast cancers (TNBCs). Furthermore, high ADAM8 levels predicted poor patient outcome. Consistently, ADAM8 promoted an aggressive phenotype of TNBC cells in culture. In a mouse orthotopic model, tumors derived from TNBC cells with ADAM8 knockdown failed to grow beyond a palpable size and displayed poor vascularization. Circulating tumor cells and brain metastases were also significantly reduced. Mechanistically, ADAM8 stimulated both angiogenesis through release of VEGF-A and transendothelial cell migration via β1-integrin activation. In vivo, treatment with an anti-ADAM8 antibody from the time of cell inoculation reduced primary tumor burden and metastases. Furthermore, antibody treatment of established tumors profoundly decreased metastases in a resection model. As a non-essential protein under physiological conditions, ADAM8 represents a promising novel target for treatment of TNBCs, which currently lack targeted therapies and frequently progress with fatal dissemination.The transmembrane metalloprotease-disintegrin ADAM8 mediates cell adhesion and shedding of ligands, receptors and extracellular matrix components. Here, we report that ADAM8 is abundantly expressed in breast tumors and derived metastases compared to normal tissue, especially in triple-negative breast cancers (TNBCs). Furthermore, high ADAM8 levels predicted poor patient outcome. Consistently, ADAM8 promoted an aggressive phenotype of TNBC cells in culture. In a mouse orthotopic model, tumors derived from TNBC cells with ADAM8 knockdown failed to grow beyond a palpable size and displayed poor vascularization. Circulating tumor cells and brain metastases were also significantly reduced. Mechanistically, ADAM8 stimulated both angiogenesis through release of VEGF-A and transendothelial cell migration via β1-integrin activation. In vivo, treatment with an anti-ADAM8 antibody from the time of cell inoculation reduced primary tumor burden and metastases. Furthermore, antibody treatment of established tumors profoundly decreased metastases in a resection model. As a non-essential protein under physiological conditions, ADAM8 represents a promising novel target for treatment of TNBCs, which currently lack targeted therapies and frequently progress with fatal dissemination. |
| Author | McDermott, Enda W Sonenshein, Gail E Polmear, Michael Parsons, Maddy Romagnoli, Mathilde Barillé‐Nion, Sophie Schlomann, Uwe Bartsch, Jörg W Conrad, Catharina McGowan, Patricia M. Georgakoudi, Irene Dagg, Áine Srinivasan, Srimathi Duffy, Michael J Mineva, Nora D Loussouarn, Delphine |
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| Keywords | breast cancer ADAM8 therapeutic target cancer progression metastasis triple‐negative triple- negative breast cancer Subject Category Cancer |
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| References_xml | – volume: 8 start-page: 464 year: 2007 end-page: 478 ident: CR1 article-title: Molecular regulation of angiogenesis and lymphangiogenesis publication-title: Nat Rev Mol Cell Biol – volume: 11 start-page: 837 year: 2005 end-page: 847 ident: CR8 article-title: ADAM‐Integrin Interactions: potential integrin regulated ectodomain shedding activity publication-title: Curr Pharm Des – volume: 40 start-page: 294 year: 2010 end-page: 309 ident: CR24 article-title: Hypoxia‐inducible factors and the response to hypoxic stress publication-title: Mol Cell – volume: 351 start-page: 781 year: 2004 end-page: 791 ident: CR9 article-title: Circulating tumor cells, disease progression, and survival in metastatic breast cancer publication-title: N Engl J Med – volume: 16 start-page: 040501 year: 2011 ident: CR17 article-title: Assessment of the role of circulating breast cancer cells in tumor formation and metastatic potential using flow cytometry publication-title: J Biomed Opt – volume: 21 start-page: 1657 year: 2006 end-page: 1665 ident: CR32 article-title: Alpha9beta1: a novel osteoclast integrin that regulates osteoclast formation and function publication-title: J Bone Miner Res – volume: 120 start-page: 2030 year: 2010 end-page: 2039 ident: CR13 article-title: Tumor cells disseminate early, but immunosurveillance limits metastatic outgrowth, in a mouse model of melanoma publication-title: J Clin Invest – volume: 96 start-page: 1092 year: 2007 end-page: 1100 ident: CR28 article-title: Prognostic significance of vascular endothelial cell growth factors ‐A, ‐C and ‐D in breast cancer and their relationship with angio‐ and lymphangiogenesis publication-title: Br J Cancer – volume: 79 start-page: 874 year: 2011 end-page: 883 ident: CR14 article-title: Confocal backscattering‐based detection of leukemic cells in flowing blood samples publication-title: Cytometry A – volume: 78 start-page: 1038 year: 2008 end-page: 1048 ident: CR39 article-title: Regulated expression of ADAM8 (a disintegrin and metalloprotease domain 8) in the mouse ovary: evidence for a regulatory role of luteinizing hormone, progesterone receptor, and epidermal growth factor‐like growth factors publication-title: Biol Reprod – volume: 21 start-page: 154 year: 2009 end-page: 165 ident: CR23 article-title: VEGFs and receptors involved in angiogenesis versus lymphangiogenesis publication-title: Curr Opin Cell Biol – volume: 2008 start-page: 183516 year: 2008 ident: CR26 article-title: Role of the endothelium during tumor cell metastasis: is the endothelium a barrier or a promoter for cell invasion and metastasis? 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Processing by autocatalysis is required for proteolytic activity and cell adhesion publication-title: J Biol Chem – volume: 12 start-page: 895 year: 2006 end-page: 904 ident: CR40 article-title: Tumor metastasis: mechanistic insights and clinical challenges publication-title: Nat Med – volume: 2 start-page: 38 year: 2002 end-page: 47 ident: CR15 article-title: Hypoxia–a key regulatory factor in tumour growth publication-title: Nat Rev Cancer – volume: 8 start-page: 9 year: 2011 ident: CR12 article-title: The ADAMs family of proteases: new biomarkers and therapeutic targets for cancer? publication-title: Clin Proteomics – volume: 44 start-page: 1904 year: 2008 end-page: 1913 ident: CR16 article-title: VEGF release by MMP‐9 mediated heparan sulphate cleavage induces colorectal cancer angiogenesis publication-title: Eur J Cancer – volume: 20 start-page: 1283 year: 2010 end-page: 1288 ident: CR30 article-title: Levels of specific glycans significantly distinguish lymph node‐positive from lymph node‐negative breast cancer patients publication-title: Glycobiology – volume: 44 start-page: 1434 year: 2011 end-page: 1439 ident: CR36 article-title: Potential of fluorescent metalloproteinase substrates for cancer detection publication-title: Clin Biochem – volume: 232 start-page: 221 year: 2005 end-page: 231 ident: CR18 article-title: Metalloprotease‐disintegrin ADAM8: expression analysis and targeted deletion in mice publication-title: Dev Dyn – volume: 2 start-page: 229 year: 2011 ident: CR25 article-title: Migration of growth factor‐stimulated epithelial and endothelial cells depends on EGFR transactivation by ADAM17 publication-title: Nat Commun – volume: 169 start-page: 681 year: 2005 end-page: 691 ident: CR20 article-title: Processing of VEGF‐A by matrix metalloproteinases regulates bioavailability and vascular patterning in tumors publication-title: J Cell Biol – volume: 130 start-page: 763 year: 2010 end-page: 773 ident: CR21 article-title: ADAM10 is upregulated in melanoma metastasis compared with primary melanoma publication-title: J Invest Dermatol – volume: 3 start-page: 401 year: 2003 end-page: 410 ident: CR5 article-title: Tumorigenesis and the angiogenic switch publication-title: Nat Rev Cancer – volume: 15 start-page: 2272 year: 2009 end-page: 2281 ident: CR19 article-title: ADAM8/MS2/CD156, an emerging drug target in the treatment of inflammatory and invasive pathologies publication-title: Curr Pharm Des – volume: 72 start-page: 6268 year: 2012 end-page: 6278 ident: CR34 article-title: Epithelial‐to‐mesenchymal transition induced by TGF‐beta1 is mediated by Blimp‐1‐dependent repression of BMP‐5 publication-title: Cancer Res – volume: 12 start-page: 445 year: 2012 end-page: 446 ident: CR38 article-title: Unifying metastasis–integrating intravasation, circulation and end‐organ colonization publication-title: Nat Rev Cancer – volume: 12 start-page: 445 year: 2012 end-page: 446 article-title: Unifying metastasis–integrating intravasation, circulation and end‐organ colonization publication-title: Nat Rev Cancer – volume: 8 start-page: 9 year: 2011 article-title: The ADAMs family of proteases: new biomarkers and therapeutic targets for cancer? publication-title: Clin Proteomics – volume: 44 start-page: 1904 year: 2008 end-page: 1913 article-title: VEGF release by MMP‐9 mediated heparan sulphate cleavage induces colorectal cancer angiogenesis publication-title: Eur J Cancer – volume: 3 start-page: 401 year: 2003 end-page: 410 article-title: Tumorigenesis and the angiogenic switch publication-title: Nat Rev Cancer – volume: 20 start-page: 1283 year: 2010 end-page: 1288 article-title: Levels of specific glycans significantly distinguish lymph node‐positive from lymph node‐negative breast cancer patients publication-title: Glycobiology – volume: 44 start-page: 1434 year: 2011b end-page: 1439 article-title: Potential of fluorescent metalloproteinase substrates for cancer detection publication-title: Clin Biochem – volume: 9 start-page: 470 year: 2007 end-page: 478 article-title: Oestrogen signalling inhibits invasive phenotype by repressing RelB and its target BCL2 publication-title: Nat Cell Biol – volume: 232 start-page: 221 year: 2005 end-page: 231 article-title: Metalloprotease‐disintegrin ADAM8: expression analysis and targeted deletion in mice publication-title: Dev Dyn – volume: 79 start-page: 874 year: 2011 end-page: 883 article-title: Confocal backscattering‐based detection of leukemic cells in flowing blood samples publication-title: Cytometry A – volume: 2 start-page: 38 year: 2002 end-page: 47 article-title: Hypoxia–a key regulatory factor in tumour growth publication-title: Nat Rev Cancer – volume: 286 start-page: 20758 year: 2011a end-page: 20768 article-title: ADAM12 transmembrane and secreted isoforms promote breast tumor growth: a distinct role for ADAM12‐S protein in tumor metastasis publication-title: J Biol Chem – volume: 11 start-page: 1162 year: 2007 end-page: 1174 article-title: ADAM8 expression is associated with increased invasiveness and reduced patient survival in pancreatic cancer publication-title: J Cell Mol Med – volume: 40 start-page: 294 year: 2010 end-page: 309 article-title: Hypoxia‐inducible factors and the response to hypoxic stress publication-title: Mol Cell – volume: 21 start-page: 154 year: 2009 end-page: 165 article-title: VEGFs and receptors involved in angiogenesis versus lymphangiogenesis publication-title: Curr Opin Cell Biol – volume: 15 start-page: 2272 year: 2009 end-page: 2281 article-title: ADAM8/MS2/CD156, an emerging drug target in the treatment of inflammatory and invasive pathologies publication-title: Curr Pharm Des – volume: 53 start-page: 229 year: 2012 end-page: 234 article-title: Immune predictors of cancer progression publication-title: Immunol Res – volume: 347 start-page: 1999 year: 2002 end-page: 2009 article-title: A gene‐expression signature as a predictor of survival in breast cancer publication-title: N Engl J Med – volume: 21 start-page: 1657 year: 2006 end-page: 1665 article-title: Alpha9beta1: a novel osteoclast integrin that regulates osteoclast formation and function publication-title: J Bone Miner Res – volume: 130 start-page: 763 year: 2010 end-page: 773 article-title: ADAM10 is upregulated in melanoma metastasis compared with primary melanoma publication-title: J Invest Dermatol – volume: 20 start-page: 1639 year: 2009 end-page: 1646 article-title: Significantly higher levels of vascular endothelial growth factor (VEGF) and shorter survival times for patients with primary operable triple‐negative breast cancer publication-title: Ann Oncol – volume: 436 start-page: 518 year: 2005 end-page: 524 article-title: Genes that mediate breast cancer metastasis to lung publication-title: Nature – volume: 11 start-page: 837 year: 2005 end-page: 847 article-title: ADAM‐Integrin Interactions: potential integrin regulated ectodomain shedding activity publication-title: Curr Pharm Des – volume: 96 start-page: 1092 year: 2007 end-page: 1100 article-title: Prognostic significance of vascular endothelial cell growth factors ‐A, ‐C and ‐D in breast cancer and their relationship with angio‐ and lymphangiogenesis publication-title: Br J Cancer – volume: 5 start-page: 1779 year: 2006 end-page: 1787 article-title: Role of angiogenesis in human tumor dormancy: animal models of the angiogenic switch publication-title: Cell Cycle – volume: 351 start-page: 781 year: 2004 end-page: 791 article-title: Circulating tumor cells, disease progression, and survival in metastatic breast cancer publication-title: N Engl J Med – volume: 2008 start-page: 183516 year: 2008 article-title: Role of the endothelium during tumor cell metastasis: is the endothelium a barrier or a promoter for cell invasion and metastasis? 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| Snippet | The transmembrane metalloprotease‐disintegrin ADAM8 mediates cell adhesion and shedding of ligands, receptors and extracellular matrix components. Here, we... The transmembrane metalloprotease-disintegrin ADAM8 mediates cell adhesion and shedding of ligands, receptors and extracellular matrix components. Here, we... Abstract The transmembrane metalloprotease‐disintegrin ADAM8 mediates cell adhesion and shedding of ligands, receptors and extracellular matrix components.... |
| SourceID | doaj pubmedcentral hal proquest pubmed wiley springer |
| SourceType | Open Website Open Access Repository Aggregation Database Index Database Publisher |
| StartPage | 278 |
| SubjectTerms | ADAM Proteins - chemistry ADAM Proteins - metabolism ADAM8 Animals Antibodies, Monoclonal - pharmacology breast cancer Breast Neoplasms - blood supply Breast Neoplasms - metabolism Breast Neoplasms - pathology Cancer cancer progression Cell Adhesion - drug effects Cell Hypoxia - drug effects Cell Movement - drug effects Cell Proliferation - drug effects EMBO03 Endothelial Cells - drug effects Endothelial Cells - metabolism Endothelial Cells - pathology Female Gene Knockdown Techniques Humans Integrin beta1 - metabolism Life Sciences Membrane Proteins - chemistry Membrane Proteins - metabolism metastasis Mice Models, Biological Neoplasm Invasiveness Neoplasm Metastasis Neoplastic Cells, Circulating - drug effects Neoplastic Cells, Circulating - metabolism Neoplastic Cells, Circulating - pathology Neovascularization, Pathologic - pathology Phenotype Prognosis Protein Structure, Tertiary Research Article therapeutic target Triple Negative Breast Neoplasms - pathology triple‐negative Tumor Cells, Cultured |
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| Title | ADAM8 expression in invasive breast cancer promotes tumor dissemination and metastasis |
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