Crosstalk between tumor and endothelial cells promotes tumor angiogenesis by MAPK activation of Notch signaling
While significant progress has been made in understanding the induction of tumor vasculature by secreted angiogenic factors, little is known regarding contact-dependent signals that promote tumor angiogenesis. Here, we report that the Notch ligand Jagged1 induced by growth factors via mitogen-activa...
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creator | Zeng, Qinghua Li, Shenglin Chepeha, Douglas B. Giordano, Thomas J. Li, Jong Zhang, Honglai Polverini, Peter J. Nor, Jacques Kitajewski, Jan Wang, Cun-Yu |
description | While significant progress has been made in understanding the induction of tumor vasculature by secreted angiogenic factors, little is known regarding contact-dependent signals that promote tumor angiogenesis. Here, we report that the Notch ligand Jagged1 induced by growth factors via mitogen-activating protein kinase (MAPK) in head and neck squamous cell carcinoma (HNSCC) cells triggered Notch activation in neighboring endothelial cells (ECs) and promoted capillary-like sprout formation. Jagged1-expressing HNSCC cells significantly enhanced neovascularization and tumor growth in vivo. Moreover, the level of Jagged1 was significantly correlated with tumor blood vessel content and associated with HNSCC development. Our results elucidate a novel mechanism by which the direct interplay between tumor cells and ECs promotes angiogenesis through MAPK and Notch signaling pathways. |
doi_str_mv | 10.1016/j.ccr.2005.06.004 |
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Here, we report that the Notch ligand Jagged1 induced by growth factors via mitogen-activating protein kinase (MAPK) in head and neck squamous cell carcinoma (HNSCC) cells triggered Notch activation in neighboring endothelial cells (ECs) and promoted capillary-like sprout formation. Jagged1-expressing HNSCC cells significantly enhanced neovascularization and tumor growth in vivo. Moreover, the level of Jagged1 was significantly correlated with tumor blood vessel content and associated with HNSCC development. Our results elucidate a novel mechanism by which the direct interplay between tumor cells and ECs promotes angiogenesis through MAPK and Notch signaling pathways.</description><identifier>ISSN: 1535-6108</identifier><identifier>EISSN: 1878-3686</identifier><identifier>DOI: 10.1016/j.ccr.2005.06.004</identifier><identifier>PMID: 16023595</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Animals ; Calcium-Binding Proteins ; Carcinoma, Squamous Cell - blood supply ; Carcinoma, Squamous Cell - pathology ; Endothelium, Vascular - metabolism ; Enzyme Activation ; Female ; Head and Neck Neoplasms - blood supply ; Head and Neck Neoplasms - pathology ; Humans ; Intercellular Signaling Peptides and Proteins ; Jagged-1 Protein ; Ligands ; Membrane Proteins - genetics ; Membrane Proteins - metabolism ; Mice ; Mice, SCID ; Mitogen-Activated Protein Kinases - metabolism ; Neoplasms - blood supply ; Neoplasms - drug therapy ; Neoplasms - pathology ; Neovascularization, Pathologic - pathology ; Receptors, Cell Surface - metabolism ; Receptors, Notch ; RNA, Small Interfering - pharmacology ; Serrate-Jagged Proteins ; Signal Transduction</subject><ispartof>Cancer cell, 2005-07, Vol.8 (1), p.13-23</ispartof><rights>2005 Elsevier Inc.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c491t-3ca65d1bbbe6bb2f0c470bb6c7b0754e10b37d4b50d25858bb36e5761ea354303</citedby><cites>FETCH-LOGICAL-c491t-3ca65d1bbbe6bb2f0c470bb6c7b0754e10b37d4b50d25858bb36e5761ea354303</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S1535610805001923$$EHTML$$P50$$Gelsevier$$Hfree_for_read</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16023595$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zeng, Qinghua</creatorcontrib><creatorcontrib>Li, Shenglin</creatorcontrib><creatorcontrib>Chepeha, Douglas B.</creatorcontrib><creatorcontrib>Giordano, Thomas J.</creatorcontrib><creatorcontrib>Li, Jong</creatorcontrib><creatorcontrib>Zhang, Honglai</creatorcontrib><creatorcontrib>Polverini, Peter J.</creatorcontrib><creatorcontrib>Nor, Jacques</creatorcontrib><creatorcontrib>Kitajewski, Jan</creatorcontrib><creatorcontrib>Wang, Cun-Yu</creatorcontrib><title>Crosstalk between tumor and endothelial cells promotes tumor angiogenesis by MAPK activation of Notch signaling</title><title>Cancer cell</title><addtitle>Cancer Cell</addtitle><description>While significant progress has been made in understanding the induction of tumor vasculature by secreted angiogenic factors, little is known regarding contact-dependent signals that promote tumor angiogenesis. Here, we report that the Notch ligand Jagged1 induced by growth factors via mitogen-activating protein kinase (MAPK) in head and neck squamous cell carcinoma (HNSCC) cells triggered Notch activation in neighboring endothelial cells (ECs) and promoted capillary-like sprout formation. Jagged1-expressing HNSCC cells significantly enhanced neovascularization and tumor growth in vivo. Moreover, the level of Jagged1 was significantly correlated with tumor blood vessel content and associated with HNSCC development. Our results elucidate a novel mechanism by which the direct interplay between tumor cells and ECs promotes angiogenesis through MAPK and Notch signaling pathways.</description><subject>Animals</subject><subject>Calcium-Binding Proteins</subject><subject>Carcinoma, Squamous Cell - blood supply</subject><subject>Carcinoma, Squamous Cell - pathology</subject><subject>Endothelium, Vascular - metabolism</subject><subject>Enzyme Activation</subject><subject>Female</subject><subject>Head and Neck Neoplasms - blood supply</subject><subject>Head and Neck Neoplasms - pathology</subject><subject>Humans</subject><subject>Intercellular Signaling Peptides and Proteins</subject><subject>Jagged-1 Protein</subject><subject>Ligands</subject><subject>Membrane Proteins - genetics</subject><subject>Membrane Proteins - metabolism</subject><subject>Mice</subject><subject>Mice, SCID</subject><subject>Mitogen-Activated Protein Kinases - metabolism</subject><subject>Neoplasms - blood supply</subject><subject>Neoplasms - drug therapy</subject><subject>Neoplasms - pathology</subject><subject>Neovascularization, Pathologic - pathology</subject><subject>Receptors, Cell Surface - metabolism</subject><subject>Receptors, Notch</subject><subject>RNA, Small Interfering - pharmacology</subject><subject>Serrate-Jagged Proteins</subject><subject>Signal Transduction</subject><issn>1535-6108</issn><issn>1878-3686</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkU9v1DAQxS0Eon_gA3BBPnFLGMexnYhTtYIWUVoOcLZsZ3brJbGL7S3qt69Xu4IbnGYOv_c08x4hbxi0DJh8v22dS20HIFqQLUD_jJyyQQ0Nl4N8XnfBRSMZDCfkLOctVA1T40tywiR0XIzilMRVijkXM_-kFstvxEDLbomJmjBRDFMsdzh7M1OH85zpfYpLLJj_QBsfNxgw-0ztI_168e0LNa74B1N8DDSu6U0s7o5mvwlm9mHzirxYmznj6-M8Jz8-ffy-umquby8_ry6uG9ePrDTcGSkmZq1FaW23BtcrsFY6ZUGJHhlYrqbeCpg6MYjBWi5RKMnQcNFz4Ofk3cG3Xvxrh7noxef9DyZg3GUtB-AjH7r_gkz1cpRcVZAdQLdPLOFa3ye_mPSoGeh9HXqrax16X4cGqWsdVfP2aL6zC05_Fcf8K_DhAGDN4sFj0tl5DA4nn9AVPUX_D_snRDCcWQ</recordid><startdate>20050701</startdate><enddate>20050701</enddate><creator>Zeng, Qinghua</creator><creator>Li, Shenglin</creator><creator>Chepeha, Douglas B.</creator><creator>Giordano, Thomas J.</creator><creator>Li, Jong</creator><creator>Zhang, Honglai</creator><creator>Polverini, Peter J.</creator><creator>Nor, Jacques</creator><creator>Kitajewski, Jan</creator><creator>Wang, Cun-Yu</creator><general>Elsevier Inc</general><scope>6I.</scope><scope>AAFTH</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7TO</scope><scope>H94</scope><scope>7X8</scope></search><sort><creationdate>20050701</creationdate><title>Crosstalk between tumor and endothelial cells promotes tumor angiogenesis by MAPK activation of Notch signaling</title><author>Zeng, Qinghua ; Li, Shenglin ; Chepeha, Douglas B. ; Giordano, Thomas J. ; Li, Jong ; Zhang, Honglai ; Polverini, Peter J. ; Nor, Jacques ; Kitajewski, Jan ; Wang, Cun-Yu</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c491t-3ca65d1bbbe6bb2f0c470bb6c7b0754e10b37d4b50d25858bb36e5761ea354303</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Animals</topic><topic>Calcium-Binding Proteins</topic><topic>Carcinoma, Squamous Cell - blood supply</topic><topic>Carcinoma, Squamous Cell - pathology</topic><topic>Endothelium, Vascular - metabolism</topic><topic>Enzyme Activation</topic><topic>Female</topic><topic>Head and Neck Neoplasms - blood supply</topic><topic>Head and Neck Neoplasms - pathology</topic><topic>Humans</topic><topic>Intercellular Signaling Peptides and Proteins</topic><topic>Jagged-1 Protein</topic><topic>Ligands</topic><topic>Membrane Proteins - genetics</topic><topic>Membrane Proteins - metabolism</topic><topic>Mice</topic><topic>Mice, SCID</topic><topic>Mitogen-Activated Protein Kinases - metabolism</topic><topic>Neoplasms - blood supply</topic><topic>Neoplasms - drug therapy</topic><topic>Neoplasms - pathology</topic><topic>Neovascularization, Pathologic - pathology</topic><topic>Receptors, Cell Surface - metabolism</topic><topic>Receptors, Notch</topic><topic>RNA, Small Interfering - pharmacology</topic><topic>Serrate-Jagged Proteins</topic><topic>Signal Transduction</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zeng, Qinghua</creatorcontrib><creatorcontrib>Li, Shenglin</creatorcontrib><creatorcontrib>Chepeha, Douglas B.</creatorcontrib><creatorcontrib>Giordano, Thomas J.</creatorcontrib><creatorcontrib>Li, Jong</creatorcontrib><creatorcontrib>Zhang, Honglai</creatorcontrib><creatorcontrib>Polverini, Peter J.</creatorcontrib><creatorcontrib>Nor, Jacques</creatorcontrib><creatorcontrib>Kitajewski, Jan</creatorcontrib><creatorcontrib>Wang, Cun-Yu</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Cancer cell</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zeng, Qinghua</au><au>Li, Shenglin</au><au>Chepeha, Douglas B.</au><au>Giordano, Thomas J.</au><au>Li, Jong</au><au>Zhang, Honglai</au><au>Polverini, Peter J.</au><au>Nor, Jacques</au><au>Kitajewski, Jan</au><au>Wang, Cun-Yu</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Crosstalk between tumor and endothelial cells promotes tumor angiogenesis by MAPK activation of Notch signaling</atitle><jtitle>Cancer cell</jtitle><addtitle>Cancer Cell</addtitle><date>2005-07-01</date><risdate>2005</risdate><volume>8</volume><issue>1</issue><spage>13</spage><epage>23</epage><pages>13-23</pages><issn>1535-6108</issn><eissn>1878-3686</eissn><abstract>While significant progress has been made in understanding the induction of tumor vasculature by secreted angiogenic factors, little is known regarding contact-dependent signals that promote tumor angiogenesis. Here, we report that the Notch ligand Jagged1 induced by growth factors via mitogen-activating protein kinase (MAPK) in head and neck squamous cell carcinoma (HNSCC) cells triggered Notch activation in neighboring endothelial cells (ECs) and promoted capillary-like sprout formation. Jagged1-expressing HNSCC cells significantly enhanced neovascularization and tumor growth in vivo. Moreover, the level of Jagged1 was significantly correlated with tumor blood vessel content and associated with HNSCC development. Our results elucidate a novel mechanism by which the direct interplay between tumor cells and ECs promotes angiogenesis through MAPK and Notch signaling pathways.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>16023595</pmid><doi>10.1016/j.ccr.2005.06.004</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Animals Calcium-Binding Proteins Carcinoma, Squamous Cell - blood supply Carcinoma, Squamous Cell - pathology Endothelium, Vascular - metabolism Enzyme Activation Female Head and Neck Neoplasms - blood supply Head and Neck Neoplasms - pathology Humans Intercellular Signaling Peptides and Proteins Jagged-1 Protein Ligands Membrane Proteins - genetics Membrane Proteins - metabolism Mice Mice, SCID Mitogen-Activated Protein Kinases - metabolism Neoplasms - blood supply Neoplasms - drug therapy Neoplasms - pathology Neovascularization, Pathologic - pathology Receptors, Cell Surface - metabolism Receptors, Notch RNA, Small Interfering - pharmacology Serrate-Jagged Proteins Signal Transduction |
title | Crosstalk between tumor and endothelial cells promotes tumor angiogenesis by MAPK activation of Notch signaling |
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