AXIN1 Expression and Localization in Meningiomas and Association to Changes of APC and E-cadherin
Tumor suppressor gene AXIN1 is an inhibitor of Wnt signaling pathway. It down-regulates the pathway's main signaling effector molecule, beta-catenin, in an AXIN-based destruction complex. In the present study we investigated the involvement of AXIN1 in intracranial meningioma. Loss of heterozyg...
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| Veröffentlicht in: | Anticancer research 2016-09, Vol.36 (9), p.4583-4594 |
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| creator | Pećina-Šlaus, Nives Kafka, Anja Vladušić, Tomislav Pećina, Hrvoje Ivan Hrašćan, Reno |
| description | Tumor suppressor gene AXIN1 is an inhibitor of Wnt signaling pathway. It down-regulates the pathway's main signaling effector molecule, beta-catenin, in an AXIN-based destruction complex. In the present study we investigated the involvement of AXIN1 in intracranial meningioma.
Loss of heterozygosity and microsatellite instability analyses were performed. The consequences of genetic changes on protein expression levels were studied in the same patients by immunohistochemistry.
Allelic deletions of AXIN1 gene were found in 21.1% of meningiomas. Microsatellite instability was also observed in 5.3% of cases. Weak or lack of AXIN1 expression was found in 21.9% of meningiomas. We found strong statistical correlations between cytoplasmic localization of AXIN1 and its weak expression and also between the simultaneous cytoplasmic and nuclear localizations and moderate and strong expression levels (p |
| doi_str_mv | 10.21873/anticanres.11007 |
| format | Article |
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Loss of heterozygosity and microsatellite instability analyses were performed. The consequences of genetic changes on protein expression levels were studied in the same patients by immunohistochemistry.
Allelic deletions of AXIN1 gene were found in 21.1% of meningiomas. Microsatellite instability was also observed in 5.3% of cases. Weak or lack of AXIN1 expression was found in 21.9% of meningiomas. We found strong statistical correlations between cytoplasmic localization of AXIN1 and its weak expression and also between the simultaneous cytoplasmic and nuclear localizations and moderate and strong expression levels (p<0.000). The findings on AXIN1 were compared to concomitant expression of APC, beta-catenin and E-cadherin in the same patients by Chi-Square tests and Pearson's correlations. Analysis revealed that AXIN1 genetic changes were significantly associated to lack of the expression of APC and presence of mutant APC proteins (p<0.018). Moderate and strong cytoplasmic and nuclear AXIN1 expressions were positively correlated to strong expression of E-cadherin (p<0.05).
Our findings on genetic changes and expression levels of AXIN1 bring novel data on its involvement in meningeal brain tumors and reveal AXIN1's relation to specific Wnt molecules.</description><identifier>ISSN: 0250-7005</identifier><identifier>EISSN: 1791-7530</identifier><identifier>DOI: 10.21873/anticanres.11007</identifier><identifier>PMID: 27630299</identifier><language>eng</language><publisher>Greece</publisher><subject>Adenomatous Polyposis Coli Protein - metabolism ; Adult ; Aged ; Alleles ; Axin Protein - metabolism ; beta Catenin - metabolism ; Brain Neoplasms - metabolism ; Cadherins - metabolism ; Cell Nucleus - metabolism ; Cytoplasm - metabolism ; Female ; Gene Deletion ; Gene Expression Regulation, Neoplastic ; Humans ; Immunohistochemistry ; Loss of Heterozygosity ; Male ; Meningioma - metabolism ; Microsatellite Repeats - genetics ; Middle Aged ; Mutation ; Signal Transduction ; Wnt Signaling Pathway</subject><ispartof>Anticancer research, 2016-09, Vol.36 (9), p.4583-4594</ispartof><rights>Copyright© 2016 International Institute of Anticancer Research (Dr. John G. Delinassios), All rights reserved.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c344t-a0c73334cf9a3f13441b21afade4c59d5056caf46c98722cd061c9b918daeb283</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27630299$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Pećina-Šlaus, Nives</creatorcontrib><creatorcontrib>Kafka, Anja</creatorcontrib><creatorcontrib>Vladušić, Tomislav</creatorcontrib><creatorcontrib>Pećina, Hrvoje Ivan</creatorcontrib><creatorcontrib>Hrašćan, Reno</creatorcontrib><title>AXIN1 Expression and Localization in Meningiomas and Association to Changes of APC and E-cadherin</title><title>Anticancer research</title><addtitle>Anticancer Res</addtitle><description>Tumor suppressor gene AXIN1 is an inhibitor of Wnt signaling pathway. It down-regulates the pathway's main signaling effector molecule, beta-catenin, in an AXIN-based destruction complex. In the present study we investigated the involvement of AXIN1 in intracranial meningioma.
Loss of heterozygosity and microsatellite instability analyses were performed. The consequences of genetic changes on protein expression levels were studied in the same patients by immunohistochemistry.
Allelic deletions of AXIN1 gene were found in 21.1% of meningiomas. Microsatellite instability was also observed in 5.3% of cases. Weak or lack of AXIN1 expression was found in 21.9% of meningiomas. We found strong statistical correlations between cytoplasmic localization of AXIN1 and its weak expression and also between the simultaneous cytoplasmic and nuclear localizations and moderate and strong expression levels (p<0.000). The findings on AXIN1 were compared to concomitant expression of APC, beta-catenin and E-cadherin in the same patients by Chi-Square tests and Pearson's correlations. Analysis revealed that AXIN1 genetic changes were significantly associated to lack of the expression of APC and presence of mutant APC proteins (p<0.018). Moderate and strong cytoplasmic and nuclear AXIN1 expressions were positively correlated to strong expression of E-cadherin (p<0.05).
Our findings on genetic changes and expression levels of AXIN1 bring novel data on its involvement in meningeal brain tumors and reveal AXIN1's relation to specific Wnt molecules.</description><subject>Adenomatous Polyposis Coli Protein - metabolism</subject><subject>Adult</subject><subject>Aged</subject><subject>Alleles</subject><subject>Axin Protein - metabolism</subject><subject>beta Catenin - metabolism</subject><subject>Brain Neoplasms - metabolism</subject><subject>Cadherins - metabolism</subject><subject>Cell Nucleus - metabolism</subject><subject>Cytoplasm - metabolism</subject><subject>Female</subject><subject>Gene Deletion</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Humans</subject><subject>Immunohistochemistry</subject><subject>Loss of Heterozygosity</subject><subject>Male</subject><subject>Meningioma - metabolism</subject><subject>Microsatellite Repeats - genetics</subject><subject>Middle Aged</subject><subject>Mutation</subject><subject>Signal Transduction</subject><subject>Wnt Signaling Pathway</subject><issn>0250-7005</issn><issn>1791-7530</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpFkLtOwzAUhi0EoqXwACwoI0vKsZ3E8RhFBSqVywASW3TiOK1RYpc4lYCnp00LTL_034aPkEsKU0ZTwW_Q9kah7bSfUgogjsiYCklDEXM4JmNgMYQCIB6RM-_fAZJEpvyUjJhIODApxwSzt_kjDWaf6-2JN84GaKtg4RQ25hv7nWFs8KCtsUvjWvRDnnnvlNnHvQvyFdql9oGrg-w5HxqzUGG10p2x5-Skxsbri4NOyOvt7CW_DxdPd_M8W4SKR1EfIijBOY9ULZHXdOvRklGssdKRimUVQ5worKNEyVQwpipIqJKlpGmFumQpn5Dr_e-6cx8b7fuiNV7ppkGr3cYXNGUQyxjErkr3VdU57ztdF-vOtNh9FRSKgWzxT7YYyG43V4f7Tdnq6m_xi5L_AKOkdqE</recordid><startdate>20160901</startdate><enddate>20160901</enddate><creator>Pećina-Šlaus, Nives</creator><creator>Kafka, Anja</creator><creator>Vladušić, Tomislav</creator><creator>Pećina, Hrvoje Ivan</creator><creator>Hrašćan, Reno</creator><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>7X8</scope></search><sort><creationdate>20160901</creationdate><title>AXIN1 Expression and Localization in Meningiomas and Association to Changes of APC and E-cadherin</title><author>Pećina-Šlaus, Nives ; Kafka, Anja ; Vladušić, Tomislav ; Pećina, Hrvoje Ivan ; Hrašćan, Reno</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c344t-a0c73334cf9a3f13441b21afade4c59d5056caf46c98722cd061c9b918daeb283</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Adenomatous Polyposis Coli Protein - metabolism</topic><topic>Adult</topic><topic>Aged</topic><topic>Alleles</topic><topic>Axin Protein - metabolism</topic><topic>beta Catenin - metabolism</topic><topic>Brain Neoplasms - metabolism</topic><topic>Cadherins - metabolism</topic><topic>Cell Nucleus - metabolism</topic><topic>Cytoplasm - metabolism</topic><topic>Female</topic><topic>Gene Deletion</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Humans</topic><topic>Immunohistochemistry</topic><topic>Loss of Heterozygosity</topic><topic>Male</topic><topic>Meningioma - metabolism</topic><topic>Microsatellite Repeats - genetics</topic><topic>Middle Aged</topic><topic>Mutation</topic><topic>Signal Transduction</topic><topic>Wnt Signaling Pathway</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Pećina-Šlaus, Nives</creatorcontrib><creatorcontrib>Kafka, Anja</creatorcontrib><creatorcontrib>Vladušić, Tomislav</creatorcontrib><creatorcontrib>Pećina, Hrvoje Ivan</creatorcontrib><creatorcontrib>Hrašćan, Reno</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Anticancer research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Pećina-Šlaus, Nives</au><au>Kafka, Anja</au><au>Vladušić, Tomislav</au><au>Pećina, Hrvoje Ivan</au><au>Hrašćan, Reno</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>AXIN1 Expression and Localization in Meningiomas and Association to Changes of APC and E-cadherin</atitle><jtitle>Anticancer research</jtitle><addtitle>Anticancer Res</addtitle><date>2016-09-01</date><risdate>2016</risdate><volume>36</volume><issue>9</issue><spage>4583</spage><epage>4594</epage><pages>4583-4594</pages><issn>0250-7005</issn><eissn>1791-7530</eissn><abstract>Tumor suppressor gene AXIN1 is an inhibitor of Wnt signaling pathway. It down-regulates the pathway's main signaling effector molecule, beta-catenin, in an AXIN-based destruction complex. In the present study we investigated the involvement of AXIN1 in intracranial meningioma.
Loss of heterozygosity and microsatellite instability analyses were performed. The consequences of genetic changes on protein expression levels were studied in the same patients by immunohistochemistry.
Allelic deletions of AXIN1 gene were found in 21.1% of meningiomas. Microsatellite instability was also observed in 5.3% of cases. Weak or lack of AXIN1 expression was found in 21.9% of meningiomas. We found strong statistical correlations between cytoplasmic localization of AXIN1 and its weak expression and also between the simultaneous cytoplasmic and nuclear localizations and moderate and strong expression levels (p<0.000). The findings on AXIN1 were compared to concomitant expression of APC, beta-catenin and E-cadherin in the same patients by Chi-Square tests and Pearson's correlations. Analysis revealed that AXIN1 genetic changes were significantly associated to lack of the expression of APC and presence of mutant APC proteins (p<0.018). Moderate and strong cytoplasmic and nuclear AXIN1 expressions were positively correlated to strong expression of E-cadherin (p<0.05).
Our findings on genetic changes and expression levels of AXIN1 bring novel data on its involvement in meningeal brain tumors and reveal AXIN1's relation to specific Wnt molecules.</abstract><cop>Greece</cop><pmid>27630299</pmid><doi>10.21873/anticanres.11007</doi><tpages>12</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Adenomatous Polyposis Coli Protein - metabolism Adult Aged Alleles Axin Protein - metabolism beta Catenin - metabolism Brain Neoplasms - metabolism Cadherins - metabolism Cell Nucleus - metabolism Cytoplasm - metabolism Female Gene Deletion Gene Expression Regulation, Neoplastic Humans Immunohistochemistry Loss of Heterozygosity Male Meningioma - metabolism Microsatellite Repeats - genetics Middle Aged Mutation Signal Transduction Wnt Signaling Pathway |
| title | AXIN1 Expression and Localization in Meningiomas and Association to Changes of APC and E-cadherin |
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