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L1CAM drives oncogenicity in esophageal squamous cell carcinoma by stimulation of ezrin transcription
L1 cell adhesion molecule (L1CAM) is highly expressed in various types of human cancers, displaying yet unknown molecular mechanisms underlying their oncogenic potential. Here, we found that L1CAM expression was significantly increased in esophageal squamous cell carcinoma (ESCC; n = 157) lesions c...
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| Published in: | Journal of molecular medicine (Berlin, Germany) Germany), 2017-12, Vol.95 (12), p.1355-1368 |
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| container_title | Journal of molecular medicine (Berlin, Germany) |
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| creator | Guo, Jin-Cheng Xie, Yang-Min Ran, Li-Qiang Cao, Hui-Hui Sun, Chun Wu, Jian-Yi Wu, Zhi-Yong Liao, Lian-Di Zhao, Wei-Jiang Fang, Wang-Kai Li, En-Min Xu, Li-Yan Schachner, Melitta Xie, Jian-Jun |
| description | L1 cell adhesion molecule (L1CAM) is highly expressed in various types of human cancers, displaying yet unknown molecular mechanisms underlying their oncogenic potential. Here, we found that L1CAM expression was significantly increased in esophageal squamous cell carcinoma (ESCC;
n
= 157) lesions compared with non-cancerous tissues. High tumorous L1CAM expression significantly correlated with reduced overall survival. Experimentally, L1CAM knockdown led to decreased cell growth, migration, and invasiveness in vitro, whereas overexpression of L1CAM showed the opposite effect. In nude mice, L1CAM depletion attenuated tumorigenesis and ability to penetrate the tissues surrounding ESCC cells. Gene set enrichment analysis (GSEA) and SubpathwayMiner analysis on gene expression profiles (microarray data on ESCC tissues, GSE53625; cDNA microarray data on L1CAM-knockdown ESCC cell line, GSE86268) suggested that L1CAM-co-expression genes were related to cell motility, cell proliferation, and regulation of actin cytoskeleton, validating the above experimental findings. Further mechanistical analysis showed that L1CAM upregulated the expression of the cytoskeletal protein ezrin via activating integrin β1/MAPK/ERK/AP1 signaling and thus led to the malignant phenotypes of ESCC cells. Together, our findings suggest that L1CAM may be employed as a valuable prognosis marker and a therapeutic target for ESCC patients and that L1CAM promotes ESCC tumorigenicity by upregulating ezrin expression.
Key messages
L1CAM promotes growth and invasiveness of ESCC cells in vitro and in vivo.
L1CAM upregulates the expression of ezrin by integrin α5β1/MAPK/ERK/AP1 pathway.
Ezrin is a key downstream effector in the L1CAM-promoted malignant phenotypes.
High expression levels of both L1CAM and ezrin significantly correlated with reduced overall survival.
Nuclear L1CAM is an independent prognosis marker for esophageal squamous cell carcinoma. |
| doi_str_mv | 10.1007/s00109-017-1595-4 |
| format | article |
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n
= 157) lesions compared with non-cancerous tissues. High tumorous L1CAM expression significantly correlated with reduced overall survival. Experimentally, L1CAM knockdown led to decreased cell growth, migration, and invasiveness in vitro, whereas overexpression of L1CAM showed the opposite effect. In nude mice, L1CAM depletion attenuated tumorigenesis and ability to penetrate the tissues surrounding ESCC cells. Gene set enrichment analysis (GSEA) and SubpathwayMiner analysis on gene expression profiles (microarray data on ESCC tissues, GSE53625; cDNA microarray data on L1CAM-knockdown ESCC cell line, GSE86268) suggested that L1CAM-co-expression genes were related to cell motility, cell proliferation, and regulation of actin cytoskeleton, validating the above experimental findings. Further mechanistical analysis showed that L1CAM upregulated the expression of the cytoskeletal protein ezrin via activating integrin β1/MAPK/ERK/AP1 signaling and thus led to the malignant phenotypes of ESCC cells. Together, our findings suggest that L1CAM may be employed as a valuable prognosis marker and a therapeutic target for ESCC patients and that L1CAM promotes ESCC tumorigenicity by upregulating ezrin expression.
Key messages
L1CAM promotes growth and invasiveness of ESCC cells in vitro and in vivo.
L1CAM upregulates the expression of ezrin by integrin α5β1/MAPK/ERK/AP1 pathway.
Ezrin is a key downstream effector in the L1CAM-promoted malignant phenotypes.
High expression levels of both L1CAM and ezrin significantly correlated with reduced overall survival.
Nuclear L1CAM is an independent prognosis marker for esophageal squamous cell carcinoma.</description><identifier>ISSN: 0946-2716</identifier><identifier>EISSN: 1432-1440</identifier><identifier>DOI: 10.1007/s00109-017-1595-4</identifier><identifier>PMID: 28939985</identifier><language>eng</language><publisher>Berlin/Heidelberg: Springer Berlin Heidelberg</publisher><subject>Actin ; Activator protein 1 ; Animal tissues ; Animals ; Base Sequence ; Biomedical and Life Sciences ; Biomedicine ; Carcinogenesis - genetics ; Carcinogenesis - pathology ; Carcinoma, Squamous Cell - genetics ; Carcinoma, Squamous Cell - pathology ; Cell adhesion ; Cell adhesion & migration ; Cell adhesion molecules ; Cell growth ; Cell Line, Tumor ; Cell Movement - genetics ; Cell proliferation ; Cell Proliferation - genetics ; Cell Survival - genetics ; Cytoskeletal Proteins - genetics ; Cytoskeletal Proteins - metabolism ; Cytoskeleton ; DNA microarrays ; Esophageal cancer ; Esophageal Neoplasms - genetics ; Esophageal Neoplasms - pathology ; Esophageal Squamous Cell Carcinoma ; Esophagus ; Ezrin ; Female ; Gene expression ; Gene Expression Regulation, Neoplastic ; Gene set enrichment analysis ; Gene Silencing ; Human Genetics ; Humans ; Internal Medicine ; Invasiveness ; Lesions ; Male ; MAP kinase ; Medical prognosis ; Mice, Nude ; Middle Aged ; Molecular Medicine ; Molecular modelling ; Multivariate Analysis ; Neoplasm Invasiveness ; Neural Cell Adhesion Molecule L1 - metabolism ; Original Article ; Phenotype ; Prognosis ; Signal Transduction - genetics ; Squamous cell carcinoma ; Subcellular Fractions - metabolism ; Transcription factors ; Transcription, Genetic ; Tumorigenesis ; Tumorigenicity ; Up-Regulation - genetics</subject><ispartof>Journal of molecular medicine (Berlin, Germany), 2017-12, Vol.95 (12), p.1355-1368</ispartof><rights>Springer-Verlag GmbH Germany 2017</rights><rights>Journal of Molecular Medicine is a copyright of Springer, (2017). All Rights Reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c372t-3e96be0916e8aab70fbb0e4a27965e8a7077269708769dea3c5b908130c58d213</citedby><cites>FETCH-LOGICAL-c372t-3e96be0916e8aab70fbb0e4a27965e8a7077269708769dea3c5b908130c58d213</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/28939985$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Guo, Jin-Cheng</creatorcontrib><creatorcontrib>Xie, Yang-Min</creatorcontrib><creatorcontrib>Ran, Li-Qiang</creatorcontrib><creatorcontrib>Cao, Hui-Hui</creatorcontrib><creatorcontrib>Sun, Chun</creatorcontrib><creatorcontrib>Wu, Jian-Yi</creatorcontrib><creatorcontrib>Wu, Zhi-Yong</creatorcontrib><creatorcontrib>Liao, Lian-Di</creatorcontrib><creatorcontrib>Zhao, Wei-Jiang</creatorcontrib><creatorcontrib>Fang, Wang-Kai</creatorcontrib><creatorcontrib>Li, En-Min</creatorcontrib><creatorcontrib>Xu, Li-Yan</creatorcontrib><creatorcontrib>Schachner, Melitta</creatorcontrib><creatorcontrib>Xie, Jian-Jun</creatorcontrib><title>L1CAM drives oncogenicity in esophageal squamous cell carcinoma by stimulation of ezrin transcription</title><title>Journal of molecular medicine (Berlin, Germany)</title><addtitle>J Mol Med</addtitle><addtitle>J Mol Med (Berl)</addtitle><description>L1 cell adhesion molecule (L1CAM) is highly expressed in various types of human cancers, displaying yet unknown molecular mechanisms underlying their oncogenic potential. Here, we found that L1CAM expression was significantly increased in esophageal squamous cell carcinoma (ESCC;
n
= 157) lesions compared with non-cancerous tissues. High tumorous L1CAM expression significantly correlated with reduced overall survival. Experimentally, L1CAM knockdown led to decreased cell growth, migration, and invasiveness in vitro, whereas overexpression of L1CAM showed the opposite effect. In nude mice, L1CAM depletion attenuated tumorigenesis and ability to penetrate the tissues surrounding ESCC cells. Gene set enrichment analysis (GSEA) and SubpathwayMiner analysis on gene expression profiles (microarray data on ESCC tissues, GSE53625; cDNA microarray data on L1CAM-knockdown ESCC cell line, GSE86268) suggested that L1CAM-co-expression genes were related to cell motility, cell proliferation, and regulation of actin cytoskeleton, validating the above experimental findings. Further mechanistical analysis showed that L1CAM upregulated the expression of the cytoskeletal protein ezrin via activating integrin β1/MAPK/ERK/AP1 signaling and thus led to the malignant phenotypes of ESCC cells. Together, our findings suggest that L1CAM may be employed as a valuable prognosis marker and a therapeutic target for ESCC patients and that L1CAM promotes ESCC tumorigenicity by upregulating ezrin expression.
Key messages
L1CAM promotes growth and invasiveness of ESCC cells in vitro and in vivo.
L1CAM upregulates the expression of ezrin by integrin α5β1/MAPK/ERK/AP1 pathway.
Ezrin is a key downstream effector in the L1CAM-promoted malignant phenotypes.
High expression levels of both L1CAM and ezrin significantly correlated with reduced overall survival.
Nuclear L1CAM is an independent prognosis marker for esophageal squamous cell carcinoma.</description><subject>Actin</subject><subject>Activator protein 1</subject><subject>Animal tissues</subject><subject>Animals</subject><subject>Base Sequence</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Carcinogenesis - genetics</subject><subject>Carcinogenesis - pathology</subject><subject>Carcinoma, Squamous Cell - genetics</subject><subject>Carcinoma, Squamous Cell - pathology</subject><subject>Cell adhesion</subject><subject>Cell adhesion & migration</subject><subject>Cell adhesion molecules</subject><subject>Cell growth</subject><subject>Cell Line, Tumor</subject><subject>Cell Movement - genetics</subject><subject>Cell proliferation</subject><subject>Cell Proliferation - genetics</subject><subject>Cell Survival - genetics</subject><subject>Cytoskeletal Proteins - genetics</subject><subject>Cytoskeletal Proteins - metabolism</subject><subject>Cytoskeleton</subject><subject>DNA microarrays</subject><subject>Esophageal cancer</subject><subject>Esophageal Neoplasms - genetics</subject><subject>Esophageal Neoplasms - pathology</subject><subject>Esophageal Squamous Cell Carcinoma</subject><subject>Esophagus</subject><subject>Ezrin</subject><subject>Female</subject><subject>Gene expression</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Gene set enrichment analysis</subject><subject>Gene Silencing</subject><subject>Human Genetics</subject><subject>Humans</subject><subject>Internal Medicine</subject><subject>Invasiveness</subject><subject>Lesions</subject><subject>Male</subject><subject>MAP kinase</subject><subject>Medical prognosis</subject><subject>Mice, Nude</subject><subject>Middle Aged</subject><subject>Molecular Medicine</subject><subject>Molecular modelling</subject><subject>Multivariate Analysis</subject><subject>Neoplasm Invasiveness</subject><subject>Neural Cell Adhesion Molecule L1 - metabolism</subject><subject>Original Article</subject><subject>Phenotype</subject><subject>Prognosis</subject><subject>Signal Transduction - genetics</subject><subject>Squamous cell carcinoma</subject><subject>Subcellular Fractions - metabolism</subject><subject>Transcription factors</subject><subject>Transcription, Genetic</subject><subject>Tumorigenesis</subject><subject>Tumorigenicity</subject><subject>Up-Regulation - genetics</subject><issn>0946-2716</issn><issn>1432-1440</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><recordid>eNp1kE1LAzEQhoMotlZ_gBcJeF6dbLKbzbEUv6DiRc8hm05ryu6mTXaF-utNqYoXTwMzz_sOPIRcMrhhAPI2AjBQGTCZsUIVmTgiYyZ4njEh4JiMQYkyyyUrR-QsxnWiZaHEKRnlleJKVcWY4JzNps90EdwHRuo761fYOev6HXUdxeg372aFpqFxO5jWD5FabBpqTbCu862h9Y7G3rVDY3rnO-qXFD9DivbBdNEGt9mvz8nJ0jQRL77nhLzd373OHrP5y8PTbDrPLJd5n3FUZY2gWImVMbWEZV0DCpNLVRZpJUHKvFQSKlmqBRpui1pBxTjYolrkjE_I9aF3E_x2wNjrtR9Cl15qpkrORcpCotiBssHHGHCpN8G1Juw0A70Xqw9idfKl92K1SJmr7-ahbnHxm_gxmYD8AMR06lYY_rz-t_ULshSD0A</recordid><startdate>20171201</startdate><enddate>20171201</enddate><creator>Guo, Jin-Cheng</creator><creator>Xie, Yang-Min</creator><creator>Ran, Li-Qiang</creator><creator>Cao, Hui-Hui</creator><creator>Sun, Chun</creator><creator>Wu, Jian-Yi</creator><creator>Wu, Zhi-Yong</creator><creator>Liao, Lian-Di</creator><creator>Zhao, Wei-Jiang</creator><creator>Fang, Wang-Kai</creator><creator>Li, En-Min</creator><creator>Xu, Li-Yan</creator><creator>Schachner, Melitta</creator><creator>Xie, Jian-Jun</creator><general>Springer Berlin Heidelberg</general><general>Springer Nature B.V</general><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>3V.</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope></search><sort><creationdate>20171201</creationdate><title>L1CAM drives oncogenicity in esophageal squamous cell carcinoma by stimulation of ezrin transcription</title><author>Guo, Jin-Cheng ; Xie, Yang-Min ; Ran, Li-Qiang ; Cao, Hui-Hui ; Sun, Chun ; Wu, Jian-Yi ; Wu, Zhi-Yong ; Liao, Lian-Di ; Zhao, Wei-Jiang ; Fang, Wang-Kai ; Li, En-Min ; Xu, Li-Yan ; Schachner, Melitta ; Xie, Jian-Jun</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c372t-3e96be0916e8aab70fbb0e4a27965e8a7077269708769dea3c5b908130c58d213</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Actin</topic><topic>Activator protein 1</topic><topic>Animal tissues</topic><topic>Animals</topic><topic>Base Sequence</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Carcinogenesis - genetics</topic><topic>Carcinogenesis - pathology</topic><topic>Carcinoma, Squamous Cell - genetics</topic><topic>Carcinoma, Squamous Cell - pathology</topic><topic>Cell adhesion</topic><topic>Cell adhesion & migration</topic><topic>Cell adhesion molecules</topic><topic>Cell growth</topic><topic>Cell Line, Tumor</topic><topic>Cell Movement - genetics</topic><topic>Cell proliferation</topic><topic>Cell Proliferation - genetics</topic><topic>Cell Survival - genetics</topic><topic>Cytoskeletal Proteins - genetics</topic><topic>Cytoskeletal Proteins - metabolism</topic><topic>Cytoskeleton</topic><topic>DNA microarrays</topic><topic>Esophageal cancer</topic><topic>Esophageal Neoplasms - genetics</topic><topic>Esophageal Neoplasms - pathology</topic><topic>Esophageal Squamous Cell Carcinoma</topic><topic>Esophagus</topic><topic>Ezrin</topic><topic>Female</topic><topic>Gene expression</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Gene set enrichment analysis</topic><topic>Gene Silencing</topic><topic>Human Genetics</topic><topic>Humans</topic><topic>Internal Medicine</topic><topic>Invasiveness</topic><topic>Lesions</topic><topic>Male</topic><topic>MAP kinase</topic><topic>Medical prognosis</topic><topic>Mice, Nude</topic><topic>Middle Aged</topic><topic>Molecular Medicine</topic><topic>Molecular modelling</topic><topic>Multivariate Analysis</topic><topic>Neoplasm Invasiveness</topic><topic>Neural Cell Adhesion Molecule L1 - metabolism</topic><topic>Original Article</topic><topic>Phenotype</topic><topic>Prognosis</topic><topic>Signal Transduction - genetics</topic><topic>Squamous cell carcinoma</topic><topic>Subcellular Fractions - metabolism</topic><topic>Transcription factors</topic><topic>Transcription, Genetic</topic><topic>Tumorigenesis</topic><topic>Tumorigenicity</topic><topic>Up-Regulation - genetics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Guo, Jin-Cheng</creatorcontrib><creatorcontrib>Xie, Yang-Min</creatorcontrib><creatorcontrib>Ran, Li-Qiang</creatorcontrib><creatorcontrib>Cao, Hui-Hui</creatorcontrib><creatorcontrib>Sun, Chun</creatorcontrib><creatorcontrib>Wu, Jian-Yi</creatorcontrib><creatorcontrib>Wu, Zhi-Yong</creatorcontrib><creatorcontrib>Liao, Lian-Di</creatorcontrib><creatorcontrib>Zhao, Wei-Jiang</creatorcontrib><creatorcontrib>Fang, Wang-Kai</creatorcontrib><creatorcontrib>Li, En-Min</creatorcontrib><creatorcontrib>Xu, Li-Yan</creatorcontrib><creatorcontrib>Schachner, Melitta</creatorcontrib><creatorcontrib>Xie, Jian-Jun</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>Neurosciences Abstracts</collection><collection>ProQuest_Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central</collection><collection>AUTh Library subscriptions: ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>PML(ProQuest Medical Library)</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><jtitle>Journal of molecular medicine (Berlin, Germany)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Guo, Jin-Cheng</au><au>Xie, Yang-Min</au><au>Ran, Li-Qiang</au><au>Cao, Hui-Hui</au><au>Sun, Chun</au><au>Wu, Jian-Yi</au><au>Wu, Zhi-Yong</au><au>Liao, Lian-Di</au><au>Zhao, Wei-Jiang</au><au>Fang, Wang-Kai</au><au>Li, En-Min</au><au>Xu, Li-Yan</au><au>Schachner, Melitta</au><au>Xie, Jian-Jun</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>L1CAM drives oncogenicity in esophageal squamous cell carcinoma by stimulation of ezrin transcription</atitle><jtitle>Journal of molecular medicine (Berlin, Germany)</jtitle><stitle>J Mol Med</stitle><addtitle>J Mol Med (Berl)</addtitle><date>2017-12-01</date><risdate>2017</risdate><volume>95</volume><issue>12</issue><spage>1355</spage><epage>1368</epage><pages>1355-1368</pages><issn>0946-2716</issn><eissn>1432-1440</eissn><abstract>L1 cell adhesion molecule (L1CAM) is highly expressed in various types of human cancers, displaying yet unknown molecular mechanisms underlying their oncogenic potential. Here, we found that L1CAM expression was significantly increased in esophageal squamous cell carcinoma (ESCC;
n
= 157) lesions compared with non-cancerous tissues. High tumorous L1CAM expression significantly correlated with reduced overall survival. Experimentally, L1CAM knockdown led to decreased cell growth, migration, and invasiveness in vitro, whereas overexpression of L1CAM showed the opposite effect. In nude mice, L1CAM depletion attenuated tumorigenesis and ability to penetrate the tissues surrounding ESCC cells. Gene set enrichment analysis (GSEA) and SubpathwayMiner analysis on gene expression profiles (microarray data on ESCC tissues, GSE53625; cDNA microarray data on L1CAM-knockdown ESCC cell line, GSE86268) suggested that L1CAM-co-expression genes were related to cell motility, cell proliferation, and regulation of actin cytoskeleton, validating the above experimental findings. Further mechanistical analysis showed that L1CAM upregulated the expression of the cytoskeletal protein ezrin via activating integrin β1/MAPK/ERK/AP1 signaling and thus led to the malignant phenotypes of ESCC cells. Together, our findings suggest that L1CAM may be employed as a valuable prognosis marker and a therapeutic target for ESCC patients and that L1CAM promotes ESCC tumorigenicity by upregulating ezrin expression.
Key messages
L1CAM promotes growth and invasiveness of ESCC cells in vitro and in vivo.
L1CAM upregulates the expression of ezrin by integrin α5β1/MAPK/ERK/AP1 pathway.
Ezrin is a key downstream effector in the L1CAM-promoted malignant phenotypes.
High expression levels of both L1CAM and ezrin significantly correlated with reduced overall survival.
Nuclear L1CAM is an independent prognosis marker for esophageal squamous cell carcinoma.</abstract><cop>Berlin/Heidelberg</cop><pub>Springer Berlin Heidelberg</pub><pmid>28939985</pmid><doi>10.1007/s00109-017-1595-4</doi><tpages>14</tpages></addata></record> |
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| ispartof | Journal of molecular medicine (Berlin, Germany), 2017-12, Vol.95 (12), p.1355-1368 |
| issn | 0946-2716 1432-1440 |
| language | eng |
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| source | Springer Nature |
| subjects | Actin Activator protein 1 Animal tissues Animals Base Sequence Biomedical and Life Sciences Biomedicine Carcinogenesis - genetics Carcinogenesis - pathology Carcinoma, Squamous Cell - genetics Carcinoma, Squamous Cell - pathology Cell adhesion Cell adhesion & migration Cell adhesion molecules Cell growth Cell Line, Tumor Cell Movement - genetics Cell proliferation Cell Proliferation - genetics Cell Survival - genetics Cytoskeletal Proteins - genetics Cytoskeletal Proteins - metabolism Cytoskeleton DNA microarrays Esophageal cancer Esophageal Neoplasms - genetics Esophageal Neoplasms - pathology Esophageal Squamous Cell Carcinoma Esophagus Ezrin Female Gene expression Gene Expression Regulation, Neoplastic Gene set enrichment analysis Gene Silencing Human Genetics Humans Internal Medicine Invasiveness Lesions Male MAP kinase Medical prognosis Mice, Nude Middle Aged Molecular Medicine Molecular modelling Multivariate Analysis Neoplasm Invasiveness Neural Cell Adhesion Molecule L1 - metabolism Original Article Phenotype Prognosis Signal Transduction - genetics Squamous cell carcinoma Subcellular Fractions - metabolism Transcription factors Transcription, Genetic Tumorigenesis Tumorigenicity Up-Regulation - genetics |
| title | L1CAM drives oncogenicity in esophageal squamous cell carcinoma by stimulation of ezrin transcription |
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