L1CAM induces perineural invasion of pancreas cancer cells by upregulation of metalloproteinase expression
Pancreas cancer cells have a tendency to invade along nerves. Such cancerous nerve invasion (CNI) is associated with poor outcome; however, the exact mechanism that drives cancer cells to disseminate along nerves is unknown. Immunohistochemical analysis of human pancreatic ductal adenocarcinoma (PDA...
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| Veröffentlicht in: | Oncogene 2019-01, Vol.38 (4), p.596-608 |
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| description | Pancreas cancer cells have a tendency to invade along nerves. Such cancerous nerve invasion (CNI) is associated with poor outcome; however, the exact mechanism that drives cancer cells to disseminate along nerves is unknown. Immunohistochemical analysis of human pancreatic ductal adenocarcinoma (PDAC) specimens showed overexpression of the L1 cell adhesion molecule (L1CAM) in cancer cells and in adjacent Schwann cells (SC) in invaded nerves. By modeling the neural microenvironment, we found that L1CAM secreted from SCs acts as a strong chemoattractant to cancer cells, through activation of MAP kinase signaling. L1CAM also upregulated expression of metalloproteinase-2 (MMP-2) and MMP-9 by PDAC cells, through STAT3 activation. Using a transgenic Pdx-1-Cre/KrasG12D /p53R172H (KPC) mouse model, we show that treatment with anti-L1CAM Ab significantly reduces CNI in vivo. We provide evidence of a paracrine response between SCs and cancer cells in the neural niche, which promotes cancer invasion via L1CAM secretion. |
| doi_str_mv | 10.1038/s41388-018-0458-y |
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Such cancerous nerve invasion (CNI) is associated with poor outcome; however, the exact mechanism that drives cancer cells to disseminate along nerves is unknown. Immunohistochemical analysis of human pancreatic ductal adenocarcinoma (PDAC) specimens showed overexpression of the L1 cell adhesion molecule (L1CAM) in cancer cells and in adjacent Schwann cells (SC) in invaded nerves. By modeling the neural microenvironment, we found that L1CAM secreted from SCs acts as a strong chemoattractant to cancer cells, through activation of MAP kinase signaling. L1CAM also upregulated expression of metalloproteinase-2 (MMP-2) and MMP-9 by PDAC cells, through STAT3 activation. Using a transgenic Pdx-1-Cre/KrasG12D /p53R172H (KPC) mouse model, we show that treatment with anti-L1CAM Ab significantly reduces CNI in vivo. We provide evidence of a paracrine response between SCs and cancer cells in the neural niche, which promotes cancer invasion via L1CAM secretion.</description><identifier>ISSN: 0950-9232</identifier><identifier>EISSN: 1476-5594</identifier><identifier>DOI: 10.1038/s41388-018-0458-y</identifier><identifier>PMID: 30171263</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>13/1 ; 13/106 ; 13/51 ; 13/89 ; 13/95 ; 14/19 ; 631/67/322 ; 631/67/327 ; 82/29 ; Adenocarcinoma ; Animals ; Apoptosis ; Cancer ; Cancer cells ; Cancer treatment ; Carcinoma, Pancreatic Ductal - enzymology ; Carcinoma, Pancreatic Ductal - genetics ; Carcinoma, Pancreatic Ductal - pathology ; Care and treatment ; Cell adhesion & migration ; Cell adhesion molecules ; Cell Biology ; Culture Media, Conditioned ; Development and progression ; Enzyme Induction - drug effects ; Gelatinase A ; Gelatinase B ; Gene expression ; Genetic aspects ; Genetic engineering ; Health aspects ; Human Genetics ; Humans ; Internal Medicine ; MAP kinase ; Medicine ; Medicine & Public Health ; Metalloproteases - biosynthesis ; Metalloproteases - genetics ; Metalloproteinase ; Mice ; Mice, Transgenic ; Neoplasm Invasiveness - physiopathology ; Neoplasm Proteins - genetics ; Neoplasm Proteins - immunology ; Neoplasm Proteins - physiology ; Nerves ; Neural Cell Adhesion Molecule L1 - genetics ; Neural Cell Adhesion Molecule L1 - immunology ; Neural Cell Adhesion Molecule L1 - physiology ; Oncology ; Pancreas ; Pancreatic cancer ; Pancreatic Neoplasms - enzymology ; Pancreatic Neoplasms - genetics ; Pancreatic Neoplasms - pathology ; Paracrine signalling ; Proteases ; RNA Interference ; RNA, Small Interfering - pharmacology ; Schwann cells ; Schwann Cells - physiology ; Stat3 protein ; Up-Regulation</subject><ispartof>Oncogene, 2019-01, Vol.38 (4), p.596-608</ispartof><rights>Springer Nature Limited 2018</rights><rights>COPYRIGHT 2019 Nature Publishing Group</rights><rights>Copyright Nature Publishing Group Jan 2019</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c505t-61b5e89d06961d71301ff9afd6493aa4ce52398549f569aa8bed4d7a4892070e3</citedby><cites>FETCH-LOGICAL-c505t-61b5e89d06961d71301ff9afd6493aa4ce52398549f569aa8bed4d7a4892070e3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30171263$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Na’ara, Shorook</creatorcontrib><creatorcontrib>Amit, Moran</creatorcontrib><creatorcontrib>Gil, Ziv</creatorcontrib><title>L1CAM induces perineural invasion of pancreas cancer cells by upregulation of metalloproteinase expression</title><title>Oncogene</title><addtitle>Oncogene</addtitle><addtitle>Oncogene</addtitle><description>Pancreas cancer cells have a tendency to invade along nerves. Such cancerous nerve invasion (CNI) is associated with poor outcome; however, the exact mechanism that drives cancer cells to disseminate along nerves is unknown. Immunohistochemical analysis of human pancreatic ductal adenocarcinoma (PDAC) specimens showed overexpression of the L1 cell adhesion molecule (L1CAM) in cancer cells and in adjacent Schwann cells (SC) in invaded nerves. By modeling the neural microenvironment, we found that L1CAM secreted from SCs acts as a strong chemoattractant to cancer cells, through activation of MAP kinase signaling. L1CAM also upregulated expression of metalloproteinase-2 (MMP-2) and MMP-9 by PDAC cells, through STAT3 activation. Using a transgenic Pdx-1-Cre/KrasG12D /p53R172H (KPC) mouse model, we show that treatment with anti-L1CAM Ab significantly reduces CNI in vivo. We provide evidence of a paracrine response between SCs and cancer cells in the neural niche, which promotes cancer invasion via L1CAM secretion.</description><subject>13/1</subject><subject>13/106</subject><subject>13/51</subject><subject>13/89</subject><subject>13/95</subject><subject>14/19</subject><subject>631/67/322</subject><subject>631/67/327</subject><subject>82/29</subject><subject>Adenocarcinoma</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>Cancer</subject><subject>Cancer cells</subject><subject>Cancer treatment</subject><subject>Carcinoma, Pancreatic Ductal - enzymology</subject><subject>Carcinoma, Pancreatic Ductal - genetics</subject><subject>Carcinoma, Pancreatic Ductal - pathology</subject><subject>Care and treatment</subject><subject>Cell adhesion & migration</subject><subject>Cell adhesion molecules</subject><subject>Cell Biology</subject><subject>Culture Media, Conditioned</subject><subject>Development and progression</subject><subject>Enzyme Induction - drug effects</subject><subject>Gelatinase A</subject><subject>Gelatinase B</subject><subject>Gene expression</subject><subject>Genetic aspects</subject><subject>Genetic engineering</subject><subject>Health aspects</subject><subject>Human Genetics</subject><subject>Humans</subject><subject>Internal Medicine</subject><subject>MAP kinase</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Metalloproteases - biosynthesis</subject><subject>Metalloproteases - genetics</subject><subject>Metalloproteinase</subject><subject>Mice</subject><subject>Mice, Transgenic</subject><subject>Neoplasm Invasiveness - physiopathology</subject><subject>Neoplasm Proteins - genetics</subject><subject>Neoplasm Proteins - immunology</subject><subject>Neoplasm Proteins - physiology</subject><subject>Nerves</subject><subject>Neural Cell Adhesion Molecule L1 - genetics</subject><subject>Neural Cell Adhesion Molecule L1 - immunology</subject><subject>Neural Cell Adhesion Molecule L1 - 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enzymology</topic><topic>Carcinoma, Pancreatic Ductal - genetics</topic><topic>Carcinoma, Pancreatic Ductal - pathology</topic><topic>Care and treatment</topic><topic>Cell adhesion & migration</topic><topic>Cell adhesion molecules</topic><topic>Cell Biology</topic><topic>Culture Media, Conditioned</topic><topic>Development and progression</topic><topic>Enzyme Induction - drug effects</topic><topic>Gelatinase A</topic><topic>Gelatinase B</topic><topic>Gene expression</topic><topic>Genetic aspects</topic><topic>Genetic engineering</topic><topic>Health aspects</topic><topic>Human Genetics</topic><topic>Humans</topic><topic>Internal Medicine</topic><topic>MAP kinase</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Metalloproteases - biosynthesis</topic><topic>Metalloproteases - genetics</topic><topic>Metalloproteinase</topic><topic>Mice</topic><topic>Mice, Transgenic</topic><topic>Neoplasm Invasiveness - physiopathology</topic><topic>Neoplasm Proteins - genetics</topic><topic>Neoplasm Proteins - immunology</topic><topic>Neoplasm Proteins - physiology</topic><topic>Nerves</topic><topic>Neural Cell Adhesion Molecule L1 - genetics</topic><topic>Neural Cell Adhesion Molecule L1 - immunology</topic><topic>Neural Cell Adhesion Molecule L1 - physiology</topic><topic>Oncology</topic><topic>Pancreas</topic><topic>Pancreatic cancer</topic><topic>Pancreatic Neoplasms - enzymology</topic><topic>Pancreatic Neoplasms - genetics</topic><topic>Pancreatic Neoplasms - pathology</topic><topic>Paracrine signalling</topic><topic>Proteases</topic><topic>RNA Interference</topic><topic>RNA, Small Interfering - pharmacology</topic><topic>Schwann cells</topic><topic>Schwann Cells - physiology</topic><topic>Stat3 protein</topic><topic>Up-Regulation</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Na’ara, Shorook</creatorcontrib><creatorcontrib>Amit, Moran</creatorcontrib><creatorcontrib>Gil, Ziv</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Biological Science Database</collection><collection>Research Library (Corporate)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>Genetics Abstracts</collection><jtitle>Oncogene</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Na’ara, Shorook</au><au>Amit, Moran</au><au>Gil, Ziv</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>L1CAM induces perineural invasion of pancreas cancer cells by upregulation of metalloproteinase expression</atitle><jtitle>Oncogene</jtitle><stitle>Oncogene</stitle><addtitle>Oncogene</addtitle><date>2019-01</date><risdate>2019</risdate><volume>38</volume><issue>4</issue><spage>596</spage><epage>608</epage><pages>596-608</pages><issn>0950-9232</issn><eissn>1476-5594</eissn><abstract>Pancreas cancer cells have a tendency to invade along nerves. Such cancerous nerve invasion (CNI) is associated with poor outcome; however, the exact mechanism that drives cancer cells to disseminate along nerves is unknown. Immunohistochemical analysis of human pancreatic ductal adenocarcinoma (PDAC) specimens showed overexpression of the L1 cell adhesion molecule (L1CAM) in cancer cells and in adjacent Schwann cells (SC) in invaded nerves. By modeling the neural microenvironment, we found that L1CAM secreted from SCs acts as a strong chemoattractant to cancer cells, through activation of MAP kinase signaling. L1CAM also upregulated expression of metalloproteinase-2 (MMP-2) and MMP-9 by PDAC cells, through STAT3 activation. Using a transgenic Pdx-1-Cre/KrasG12D /p53R172H (KPC) mouse model, we show that treatment with anti-L1CAM Ab significantly reduces CNI in vivo. We provide evidence of a paracrine response between SCs and cancer cells in the neural niche, which promotes cancer invasion via L1CAM secretion.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>30171263</pmid><doi>10.1038/s41388-018-0458-y</doi><tpages>13</tpages></addata></record> |
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| subjects | 13/1 13/106 13/51 13/89 13/95 14/19 631/67/322 631/67/327 82/29 Adenocarcinoma Animals Apoptosis Cancer Cancer cells Cancer treatment Carcinoma, Pancreatic Ductal - enzymology Carcinoma, Pancreatic Ductal - genetics Carcinoma, Pancreatic Ductal - pathology Care and treatment Cell adhesion & migration Cell adhesion molecules Cell Biology Culture Media, Conditioned Development and progression Enzyme Induction - drug effects Gelatinase A Gelatinase B Gene expression Genetic aspects Genetic engineering Health aspects Human Genetics Humans Internal Medicine MAP kinase Medicine Medicine & Public Health Metalloproteases - biosynthesis Metalloproteases - genetics Metalloproteinase Mice Mice, Transgenic Neoplasm Invasiveness - physiopathology Neoplasm Proteins - genetics Neoplasm Proteins - immunology Neoplasm Proteins - physiology Nerves Neural Cell Adhesion Molecule L1 - genetics Neural Cell Adhesion Molecule L1 - immunology Neural Cell Adhesion Molecule L1 - physiology Oncology Pancreas Pancreatic cancer Pancreatic Neoplasms - enzymology Pancreatic Neoplasms - genetics Pancreatic Neoplasms - pathology Paracrine signalling Proteases RNA Interference RNA, Small Interfering - pharmacology Schwann cells Schwann Cells - physiology Stat3 protein Up-Regulation |
| title | L1CAM induces perineural invasion of pancreas cancer cells by upregulation of metalloproteinase expression |
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