Adherens junctional associated protein-1: A novel 1p36 tumor suppressor candidate in gliomas
In a broad range of human cancers 1p36 has been a mutational hotspot which strongly suggests that the loss of tumor suppressor activity maps to this genomic region during tumorigenesis. Adherens junctional associated protein-1 (AJAP1; also known as Shrew1) was initially discovered as a novel transme...
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| Veröffentlicht in: | International journal of oncology 2014-07, Vol.45 (1), p.13-17 |
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| creator | ZENG, LIANG FEE, BRIAN E RIVAS, MIRIAM V LIN, JAMES ADAMSON, DAVID CORY |
| description | In a broad range of human cancers 1p36 has been a mutational hotspot which strongly suggests that the loss of tumor suppressor activity maps to this genomic region during tumorigenesis. Adherens junctional associated protein-1 (AJAP1; also known as Shrew1) was initially discovered as a novel transmembrane protein of adherent junctions in epithelial cells. Gene profiling showed AJAP1 on 1p36 is frequently lost or epigenetically silenced. AJAP1 may affect cell motility, migration, invasion and proliferation by unclear mechanisms. AJAP1 may be translocated to the nucleus, via its interaction with β-catenin complexes, where it can regulate gene transcription, then possibly have a potent impact on cell cycling and apoptosis. Significantly, loss of AJAP1 expression predicts poor clinical outcome of patients with malignant gliomas such as GBM and it may serve as a promising tumor suppressor-related target. In this review, we summarize and discuss current knowledge that may identify AJAP1 as a tumor suppressor in gliomas. |
| doi_str_mv | 10.3892/ijo.2014.2425 |
| format | Article |
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Adherens junctional associated protein-1 (AJAP1; also known as Shrew1) was initially discovered as a novel transmembrane protein of adherent junctions in epithelial cells. Gene profiling showed AJAP1 on 1p36 is frequently lost or epigenetically silenced. AJAP1 may affect cell motility, migration, invasion and proliferation by unclear mechanisms. AJAP1 may be translocated to the nucleus, via its interaction with β-catenin complexes, where it can regulate gene transcription, then possibly have a potent impact on cell cycling and apoptosis. Significantly, loss of AJAP1 expression predicts poor clinical outcome of patients with malignant gliomas such as GBM and it may serve as a promising tumor suppressor-related target. In this review, we summarize and discuss current knowledge that may identify AJAP1 as a tumor suppressor in gliomas.</description><identifier>ISSN: 1019-6439</identifier><identifier>EISSN: 1791-2423</identifier><identifier>DOI: 10.3892/ijo.2014.2425</identifier><identifier>PMID: 24807315</identifier><language>eng</language><publisher>Greece: D.A. Spandidos</publisher><subject>adherens junctions-associated protein ; Apoptosis ; Brain cancer ; Cell adhesion & migration ; Cell Adhesion Molecules - genetics ; Cell Adhesion Molecules - metabolism ; Cell junctions ; Chromosomes, Human, Pair 1 - metabolism ; Epigenesis, Genetic ; Epigenetics ; Gene Deletion ; Gene expression ; Gene Silencing ; Glioma ; Glioma - genetics ; Glioma - pathology ; Gliomas ; Health aspects ; Humans ; Junctional complexes (Epithelium) ; Medical prognosis ; Motility ; Mutation ; Nervous system ; Neuroblastoma ; Physiological aspects ; Proteins ; Studies ; Tumor proteins ; tumor suppressor ; Tumor Suppressor Proteins - genetics ; Tumor Suppressor Proteins - metabolism ; Tumorigenesis ; Tumors</subject><ispartof>International journal of oncology, 2014-07, Vol.45 (1), p.13-17</ispartof><rights>Copyright © 2014, Spandidos Publications</rights><rights>COPYRIGHT 2014 Spandidos Publications</rights><rights>Copyright Spandidos Publications UK Ltd. 2014</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c490t-db741a0ec9de6c7dc084ef63fe4843bef58a15838099d8395db4e574e71d16c13</citedby><cites>FETCH-LOGICAL-c490t-db741a0ec9de6c7dc084ef63fe4843bef58a15838099d8395db4e574e71d16c13</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,5571,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24807315$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>ZENG, LIANG</creatorcontrib><creatorcontrib>FEE, BRIAN E</creatorcontrib><creatorcontrib>RIVAS, MIRIAM V</creatorcontrib><creatorcontrib>LIN, JAMES</creatorcontrib><creatorcontrib>ADAMSON, DAVID CORY</creatorcontrib><title>Adherens junctional associated protein-1: A novel 1p36 tumor suppressor candidate in gliomas</title><title>International journal of oncology</title><addtitle>Int J Oncol</addtitle><description>In a broad range of human cancers 1p36 has been a mutational hotspot which strongly suggests that the loss of tumor suppressor activity maps to this genomic region during tumorigenesis. Adherens junctional associated protein-1 (AJAP1; also known as Shrew1) was initially discovered as a novel transmembrane protein of adherent junctions in epithelial cells. Gene profiling showed AJAP1 on 1p36 is frequently lost or epigenetically silenced. AJAP1 may affect cell motility, migration, invasion and proliferation by unclear mechanisms. AJAP1 may be translocated to the nucleus, via its interaction with β-catenin complexes, where it can regulate gene transcription, then possibly have a potent impact on cell cycling and apoptosis. Significantly, loss of AJAP1 expression predicts poor clinical outcome of patients with malignant gliomas such as GBM and it may serve as a promising tumor suppressor-related target. In this review, we summarize and discuss current knowledge that may identify AJAP1 as a tumor suppressor in gliomas.</description><subject>adherens junctions-associated protein</subject><subject>Apoptosis</subject><subject>Brain cancer</subject><subject>Cell adhesion & migration</subject><subject>Cell Adhesion Molecules - genetics</subject><subject>Cell Adhesion Molecules - metabolism</subject><subject>Cell junctions</subject><subject>Chromosomes, Human, Pair 1 - metabolism</subject><subject>Epigenesis, Genetic</subject><subject>Epigenetics</subject><subject>Gene Deletion</subject><subject>Gene expression</subject><subject>Gene Silencing</subject><subject>Glioma</subject><subject>Glioma - genetics</subject><subject>Glioma - pathology</subject><subject>Gliomas</subject><subject>Health aspects</subject><subject>Humans</subject><subject>Junctional complexes (Epithelium)</subject><subject>Medical prognosis</subject><subject>Motility</subject><subject>Mutation</subject><subject>Nervous system</subject><subject>Neuroblastoma</subject><subject>Physiological aspects</subject><subject>Proteins</subject><subject>Studies</subject><subject>Tumor proteins</subject><subject>tumor suppressor</subject><subject>Tumor Suppressor Proteins - genetics</subject><subject>Tumor Suppressor Proteins - metabolism</subject><subject>Tumorigenesis</subject><subject>Tumors</subject><issn>1019-6439</issn><issn>1791-2423</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNptkcuLFDEQh4Mo7kOPXiUg6Cljnt2Jt2HxBQte9CaETFK9k6E7aZNuYf97M866uiA5pAjfr0jVh9ALRjdCG_42HvKGUyY3XHL1CJ2z3jDSavG41ZQZ0klhztBFrQdKuVKUPUVnXGraC6bO0fdt2EOBVPFhTX6JObkRu1qzj26BgOeSF4iJsHd4i1P-CSNms-jwsk654LrOc4FGF-xdCjG0DI4J34wxT64-Q08GN1Z4fndfom8f3n-9-kSuv3z8fLW9Jl4aupCw6yVzFLwJ0Pk-eKolDJ0YQGopdjAo7ZjSQlNjghZGhZ0E1UvoWWCdZ-ISvTr1bb_9sUJd7CGvpU1SLTOC617ITv2lbtwINqYhL8X5KVZvt5J33EhldKM2_6HaCTBFnxMMsb0_CLz-J7AHNy77msf1uMv6ECQn0Jdca4HBziVOrtxaRu3RpW0u7dGlPbps_Mu7qdbdBOGe_iOvAW9OQJ1_Lz_Xe6Z1IlIRygilTIhfrgykfA</recordid><startdate>20140701</startdate><enddate>20140701</enddate><creator>ZENG, LIANG</creator><creator>FEE, BRIAN E</creator><creator>RIVAS, MIRIAM V</creator><creator>LIN, JAMES</creator><creator>ADAMSON, DAVID CORY</creator><general>D.A. 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genetics</topic><topic>Cell Adhesion Molecules - metabolism</topic><topic>Cell junctions</topic><topic>Chromosomes, Human, Pair 1 - metabolism</topic><topic>Epigenesis, Genetic</topic><topic>Epigenetics</topic><topic>Gene Deletion</topic><topic>Gene expression</topic><topic>Gene Silencing</topic><topic>Glioma</topic><topic>Glioma - genetics</topic><topic>Glioma - pathology</topic><topic>Gliomas</topic><topic>Health aspects</topic><topic>Humans</topic><topic>Junctional complexes (Epithelium)</topic><topic>Medical prognosis</topic><topic>Motility</topic><topic>Mutation</topic><topic>Nervous system</topic><topic>Neuroblastoma</topic><topic>Physiological aspects</topic><topic>Proteins</topic><topic>Studies</topic><topic>Tumor proteins</topic><topic>tumor suppressor</topic><topic>Tumor Suppressor Proteins - genetics</topic><topic>Tumor Suppressor Proteins - metabolism</topic><topic>Tumorigenesis</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>ZENG, LIANG</creatorcontrib><creatorcontrib>FEE, BRIAN E</creatorcontrib><creatorcontrib>RIVAS, MIRIAM V</creatorcontrib><creatorcontrib>LIN, JAMES</creatorcontrib><creatorcontrib>ADAMSON, DAVID CORY</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>Nursing & Allied Health Database</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</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 Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>British Nursing Database</collection><collection>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>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Nursing & Allied Health Premium</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>International journal of oncology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>ZENG, LIANG</au><au>FEE, BRIAN E</au><au>RIVAS, MIRIAM V</au><au>LIN, JAMES</au><au>ADAMSON, DAVID CORY</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Adherens junctional associated protein-1: A novel 1p36 tumor suppressor candidate in gliomas</atitle><jtitle>International journal of oncology</jtitle><addtitle>Int J Oncol</addtitle><date>2014-07-01</date><risdate>2014</risdate><volume>45</volume><issue>1</issue><spage>13</spage><epage>17</epage><pages>13-17</pages><issn>1019-6439</issn><eissn>1791-2423</eissn><abstract>In a broad range of human cancers 1p36 has been a mutational hotspot which strongly suggests that the loss of tumor suppressor activity maps to this genomic region during tumorigenesis. Adherens junctional associated protein-1 (AJAP1; also known as Shrew1) was initially discovered as a novel transmembrane protein of adherent junctions in epithelial cells. Gene profiling showed AJAP1 on 1p36 is frequently lost or epigenetically silenced. AJAP1 may affect cell motility, migration, invasion and proliferation by unclear mechanisms. AJAP1 may be translocated to the nucleus, via its interaction with β-catenin complexes, where it can regulate gene transcription, then possibly have a potent impact on cell cycling and apoptosis. Significantly, loss of AJAP1 expression predicts poor clinical outcome of patients with malignant gliomas such as GBM and it may serve as a promising tumor suppressor-related target. In this review, we summarize and discuss current knowledge that may identify AJAP1 as a tumor suppressor in gliomas.</abstract><cop>Greece</cop><pub>D.A. 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| subjects | adherens junctions-associated protein Apoptosis Brain cancer Cell adhesion & migration Cell Adhesion Molecules - genetics Cell Adhesion Molecules - metabolism Cell junctions Chromosomes, Human, Pair 1 - metabolism Epigenesis, Genetic Epigenetics Gene Deletion Gene expression Gene Silencing Glioma Glioma - genetics Glioma - pathology Gliomas Health aspects Humans Junctional complexes (Epithelium) Medical prognosis Motility Mutation Nervous system Neuroblastoma Physiological aspects Proteins Studies Tumor proteins tumor suppressor Tumor Suppressor Proteins - genetics Tumor Suppressor Proteins - metabolism Tumorigenesis Tumors |
| title | Adherens junctional associated protein-1: A novel 1p36 tumor suppressor candidate in gliomas |
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