Effect of aspirin on the Wnt/β-catenin pathway is mediated via protein phosphatase 2A
Nonsteroidal anti-inflammatory drugs show chemopreventive efficacy in colon cancer, but the mechanism behind this remains unclear. Elucidating this mechanism is seen as vital to the development of new chemopreventive agents. We studied the effects of aspirin on the oncogenic Wnt/ β -catenin pathway...
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| Veröffentlicht in: | Oncogene 2006-10, Vol.25 (49), p.6447-6456 |
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| creator | Bos, C L Kodach, L L van den Brink, G R Diks, S H van Santen, M M Richel, D J Peppelenbosch, M P Hardwick, J C H |
| description | Nonsteroidal anti-inflammatory drugs show chemopreventive efficacy in colon cancer, but the mechanism behind this remains unclear. Elucidating this mechanism is seen as vital to the development of new chemopreventive agents. We studied the effects of aspirin on the oncogenic Wnt/
β
-catenin pathway activity in colorectal cancer cell lines and observed that aspirin dose-dependently decreased the activity of this pathway, as judged by TCF-driven luciferase activity, reduced Wnt target gene expression and increased phosphorylation of
β
-catenin by immunoblotting. Furthermore, the ubiquitination and cytoplasmic levels of
β
-catenin were assessed by immunoblotting, and also the localization of
β
-catenin was shown by green fluorescent protein-tagged
β
-catenin and time-lapse fluorescent imaging. Importantly, aspirin treatment caused increased phosphorylation of protein phosphatase 2A (PP2A), an event associated with inhibition of PP2A enzymatic activity, which was confirmed by a reduction in enzymatic PP2A activity. Moreover, this inhibition of PP2A enzymatic activity was essential for the effects of aspirin on the Wnt/
β
-catenin pathway as shown by transient transfection with PP2A constructs. The findings in this article provide a molecular explanation for the efficacy of aspirin in chemoprevention of colorectal cancer and shows biochemical evidence that PP2A is an important regulator of Wnt/
β
-catenin pathway activity in these cells. |
| doi_str_mv | 10.1038/sj.onc.1209658 |
| format | Article |
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β
-catenin pathway activity in colorectal cancer cell lines and observed that aspirin dose-dependently decreased the activity of this pathway, as judged by TCF-driven luciferase activity, reduced Wnt target gene expression and increased phosphorylation of
β
-catenin by immunoblotting. Furthermore, the ubiquitination and cytoplasmic levels of
β
-catenin were assessed by immunoblotting, and also the localization of
β
-catenin was shown by green fluorescent protein-tagged
β
-catenin and time-lapse fluorescent imaging. Importantly, aspirin treatment caused increased phosphorylation of protein phosphatase 2A (PP2A), an event associated with inhibition of PP2A enzymatic activity, which was confirmed by a reduction in enzymatic PP2A activity. Moreover, this inhibition of PP2A enzymatic activity was essential for the effects of aspirin on the Wnt/
β
-catenin pathway as shown by transient transfection with PP2A constructs. The findings in this article provide a molecular explanation for the efficacy of aspirin in chemoprevention of colorectal cancer and shows biochemical evidence that PP2A is an important regulator of Wnt/
β
-catenin pathway activity in these cells.</description><identifier>ISSN: 0950-9232</identifier><identifier>EISSN: 1476-5594</identifier><identifier>DOI: 10.1038/sj.onc.1209658</identifier><identifier>PMID: 16878161</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>Anaphase-Promoting Complex-Cyclosome ; Anti-inflammatory agents ; Anti-Inflammatory Agents, Non-Steroidal - pharmacology ; Apoptosis ; Aspirin ; Aspirin - pharmacology ; beta Catenin - metabolism ; Biological and medical sciences ; Cell Biology ; Cell physiology ; Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes ; Chemopreventive agents ; Colon cancer ; Colorectal cancer ; Colorectal carcinoma ; Cytoplasm - metabolism ; Down-Regulation - drug effects ; Enzymatic activity ; Fundamental and applied biological sciences. Psychology ; Gastroenterology. Liver. Pancreas. Abdomen ; Gene expression ; Gene Expression Regulation, Neoplastic - drug effects ; Genes, Reporter - drug effects ; Green fluorescent protein ; HCT116 Cells ; Human Genetics ; Humans ; Immunoblotting ; Inflammation ; Internal Medicine ; Localization ; Medical sciences ; Medicine ; Medicine & Public Health ; Molecular and cellular biology ; Oncology ; original-article ; Phosphatase ; Phosphoprotein phosphatase ; Phosphoprotein Phosphatases - metabolism ; Phosphoprotein Phosphatases - physiology ; Phosphorylation ; Phosphorylation - drug effects ; Protein phosphatase ; Protein Phosphatase 2 ; Protein Processing, Post-Translational - drug effects ; Proteins ; Signal Transduction - drug effects ; Stomach. Duodenum. Small intestine. Colon. Rectum. Anus ; TCF Transcription Factors - metabolism ; Transfection ; Tumor cell lines ; Tumor Cells, Cultured ; Tumors ; Ubiquitin - metabolism ; Ubiquitin-Protein Ligase Complexes - genetics ; Ubiquitination ; Wnt protein ; Wnt Proteins - metabolism ; β-Catenin</subject><ispartof>Oncogene, 2006-10, Vol.25 (49), p.6447-6456</ispartof><rights>Springer Nature Limited 2006</rights><rights>2006 INIST-CNRS</rights><rights>COPYRIGHT 2006 Nature Publishing Group</rights><rights>Nature Publishing Group 2006.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c458t-1bbb62897a477820118b2c1eebc32689dc42346d7c4da22673dff24cf2b6a2433</citedby><cites>FETCH-LOGICAL-c458t-1bbb62897a477820118b2c1eebc32689dc42346d7c4da22673dff24cf2b6a2433</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>315,781,785,27925,27926</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=18213628$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16878161$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Bos, C L</creatorcontrib><creatorcontrib>Kodach, L L</creatorcontrib><creatorcontrib>van den Brink, G R</creatorcontrib><creatorcontrib>Diks, S H</creatorcontrib><creatorcontrib>van Santen, M M</creatorcontrib><creatorcontrib>Richel, D J</creatorcontrib><creatorcontrib>Peppelenbosch, M P</creatorcontrib><creatorcontrib>Hardwick, J C H</creatorcontrib><title>Effect of aspirin on the Wnt/β-catenin pathway is mediated via protein phosphatase 2A</title><title>Oncogene</title><addtitle>Oncogene</addtitle><addtitle>Oncogene</addtitle><description>Nonsteroidal anti-inflammatory drugs show chemopreventive efficacy in colon cancer, but the mechanism behind this remains unclear. Elucidating this mechanism is seen as vital to the development of new chemopreventive agents. We studied the effects of aspirin on the oncogenic Wnt/
β
-catenin pathway activity in colorectal cancer cell lines and observed that aspirin dose-dependently decreased the activity of this pathway, as judged by TCF-driven luciferase activity, reduced Wnt target gene expression and increased phosphorylation of
β
-catenin by immunoblotting. Furthermore, the ubiquitination and cytoplasmic levels of
β
-catenin were assessed by immunoblotting, and also the localization of
β
-catenin was shown by green fluorescent protein-tagged
β
-catenin and time-lapse fluorescent imaging. Importantly, aspirin treatment caused increased phosphorylation of protein phosphatase 2A (PP2A), an event associated with inhibition of PP2A enzymatic activity, which was confirmed by a reduction in enzymatic PP2A activity. Moreover, this inhibition of PP2A enzymatic activity was essential for the effects of aspirin on the Wnt/
β
-catenin pathway as shown by transient transfection with PP2A constructs. The findings in this article provide a molecular explanation for the efficacy of aspirin in chemoprevention of colorectal cancer and shows biochemical evidence that PP2A is an important regulator of Wnt/
β
-catenin pathway activity in these cells.</description><subject>Anaphase-Promoting Complex-Cyclosome</subject><subject>Anti-inflammatory agents</subject><subject>Anti-Inflammatory Agents, Non-Steroidal - pharmacology</subject><subject>Apoptosis</subject><subject>Aspirin</subject><subject>Aspirin - pharmacology</subject><subject>beta Catenin - metabolism</subject><subject>Biological and medical sciences</subject><subject>Cell Biology</subject><subject>Cell physiology</subject><subject>Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes</subject><subject>Chemopreventive agents</subject><subject>Colon cancer</subject><subject>Colorectal cancer</subject><subject>Colorectal carcinoma</subject><subject>Cytoplasm - metabolism</subject><subject>Down-Regulation - drug effects</subject><subject>Enzymatic activity</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Gastroenterology. Liver. Pancreas. Abdomen</subject><subject>Gene expression</subject><subject>Gene Expression Regulation, Neoplastic - drug effects</subject><subject>Genes, Reporter - drug effects</subject><subject>Green fluorescent protein</subject><subject>HCT116 Cells</subject><subject>Human Genetics</subject><subject>Humans</subject><subject>Immunoblotting</subject><subject>Inflammation</subject><subject>Internal Medicine</subject><subject>Localization</subject><subject>Medical sciences</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Molecular and cellular biology</subject><subject>Oncology</subject><subject>original-article</subject><subject>Phosphatase</subject><subject>Phosphoprotein phosphatase</subject><subject>Phosphoprotein Phosphatases - metabolism</subject><subject>Phosphoprotein Phosphatases - physiology</subject><subject>Phosphorylation</subject><subject>Phosphorylation - drug effects</subject><subject>Protein phosphatase</subject><subject>Protein Phosphatase 2</subject><subject>Protein Processing, Post-Translational - drug effects</subject><subject>Proteins</subject><subject>Signal Transduction - drug effects</subject><subject>Stomach. Duodenum. Small intestine. Colon. Rectum. Anus</subject><subject>TCF Transcription Factors - metabolism</subject><subject>Transfection</subject><subject>Tumor cell lines</subject><subject>Tumor Cells, Cultured</subject><subject>Tumors</subject><subject>Ubiquitin - metabolism</subject><subject>Ubiquitin-Protein Ligase Complexes - genetics</subject><subject>Ubiquitination</subject><subject>Wnt protein</subject><subject>Wnt Proteins - metabolism</subject><subject>β-Catenin</subject><issn>0950-9232</issn><issn>1476-5594</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNp1kUuLFDEQx4Mo7rh69SgB0VvP5NV5HIdlfcCCFx_HkE4nOxl6kjbJrOzX8oP4mcywDQOykkOg6ldV_6o_AK8xWmNE5abs1ynaNSZI8V4-ASvMBO_6XrGnYIVUjzpFKLkAL0rZI4SEQuQ5uMBcCok5XoHv1947W2Hy0JQ55BBhirDuHPwR6-bP786a6mKLzqbufpl7GAo8uDG06AjvgoFzTtWd8rtU5p2ppjhIti_BM2-m4l4t_yX49uH669Wn7ubLx89X25vOsl7WDg_DwIlUwjAhJEEYy4FY7NxgKeFSjZYRyvgoLBsNIVzQ0XvCrCcDN4RRegneP_RtMn4eXan6EIp102SiS8eiWw_RliYNfPsPuE_HHJs2TTjDVDAu-Jm6NZPTIfpUs7GnlnqLpUI9Y4o1av0I1d7oDsGm6Hxo8ccKbE6lZOf1nMPB5HuNkT7ZqMteNxv1YmMreLOoPQ7t2md88a0B7xbAFGsmn020oZw5STBth23c5oErLRVvXT6v_Z_RfwFbiLPB</recordid><startdate>20061019</startdate><enddate>20061019</enddate><creator>Bos, C L</creator><creator>Kodach, L L</creator><creator>van den Brink, G R</creator><creator>Diks, S H</creator><creator>van Santen, M M</creator><creator>Richel, D J</creator><creator>Peppelenbosch, M P</creator><creator>Hardwick, J C H</creator><general>Nature Publishing Group UK</general><general>Nature Publishing</general><general>Nature Publishing Group</general><scope>IQODW</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>3V.</scope><scope>7TM</scope><scope>7TO</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>M7P</scope><scope>MBDVC</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>20061019</creationdate><title>Effect of aspirin on the Wnt/β-catenin pathway is mediated via protein phosphatase 2A</title><author>Bos, C L ; Kodach, L L ; van den Brink, G R ; Diks, S H ; van Santen, M M ; Richel, D J ; Peppelenbosch, M P ; Hardwick, J C H</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c458t-1bbb62897a477820118b2c1eebc32689dc42346d7c4da22673dff24cf2b6a2433</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>Anaphase-Promoting Complex-Cyclosome</topic><topic>Anti-inflammatory agents</topic><topic>Anti-Inflammatory Agents, Non-Steroidal - pharmacology</topic><topic>Apoptosis</topic><topic>Aspirin</topic><topic>Aspirin - pharmacology</topic><topic>beta Catenin - metabolism</topic><topic>Biological and medical sciences</topic><topic>Cell Biology</topic><topic>Cell physiology</topic><topic>Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes</topic><topic>Chemopreventive agents</topic><topic>Colon cancer</topic><topic>Colorectal cancer</topic><topic>Colorectal carcinoma</topic><topic>Cytoplasm - metabolism</topic><topic>Down-Regulation - drug effects</topic><topic>Enzymatic activity</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Gastroenterology. Liver. Pancreas. Abdomen</topic><topic>Gene expression</topic><topic>Gene Expression Regulation, Neoplastic - drug effects</topic><topic>Genes, Reporter - drug effects</topic><topic>Green fluorescent protein</topic><topic>HCT116 Cells</topic><topic>Human Genetics</topic><topic>Humans</topic><topic>Immunoblotting</topic><topic>Inflammation</topic><topic>Internal Medicine</topic><topic>Localization</topic><topic>Medical sciences</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Molecular and cellular biology</topic><topic>Oncology</topic><topic>original-article</topic><topic>Phosphatase</topic><topic>Phosphoprotein phosphatase</topic><topic>Phosphoprotein Phosphatases - metabolism</topic><topic>Phosphoprotein Phosphatases - physiology</topic><topic>Phosphorylation</topic><topic>Phosphorylation - drug effects</topic><topic>Protein phosphatase</topic><topic>Protein Phosphatase 2</topic><topic>Protein Processing, Post-Translational - drug effects</topic><topic>Proteins</topic><topic>Signal Transduction - drug effects</topic><topic>Stomach. Duodenum. Small intestine. Colon. Rectum. Anus</topic><topic>TCF Transcription Factors - metabolism</topic><topic>Transfection</topic><topic>Tumor cell lines</topic><topic>Tumor Cells, Cultured</topic><topic>Tumors</topic><topic>Ubiquitin - metabolism</topic><topic>Ubiquitin-Protein Ligase Complexes - genetics</topic><topic>Ubiquitination</topic><topic>Wnt protein</topic><topic>Wnt Proteins - metabolism</topic><topic>β-Catenin</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Bos, C L</creatorcontrib><creatorcontrib>Kodach, L L</creatorcontrib><creatorcontrib>van den Brink, G R</creatorcontrib><creatorcontrib>Diks, S H</creatorcontrib><creatorcontrib>van Santen, M M</creatorcontrib><creatorcontrib>Richel, D J</creatorcontrib><creatorcontrib>Peppelenbosch, M P</creatorcontrib><creatorcontrib>Hardwick, J C H</creatorcontrib><collection>Pascal-Francis</collection><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><collection>MEDLINE - Academic</collection><jtitle>Oncogene</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Bos, C L</au><au>Kodach, L L</au><au>van den Brink, G R</au><au>Diks, S H</au><au>van Santen, M M</au><au>Richel, D J</au><au>Peppelenbosch, M P</au><au>Hardwick, J C H</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Effect of aspirin on the Wnt/β-catenin pathway is mediated via protein phosphatase 2A</atitle><jtitle>Oncogene</jtitle><stitle>Oncogene</stitle><addtitle>Oncogene</addtitle><date>2006-10-19</date><risdate>2006</risdate><volume>25</volume><issue>49</issue><spage>6447</spage><epage>6456</epage><pages>6447-6456</pages><issn>0950-9232</issn><eissn>1476-5594</eissn><abstract>Nonsteroidal anti-inflammatory drugs show chemopreventive efficacy in colon cancer, but the mechanism behind this remains unclear. Elucidating this mechanism is seen as vital to the development of new chemopreventive agents. We studied the effects of aspirin on the oncogenic Wnt/
β
-catenin pathway activity in colorectal cancer cell lines and observed that aspirin dose-dependently decreased the activity of this pathway, as judged by TCF-driven luciferase activity, reduced Wnt target gene expression and increased phosphorylation of
β
-catenin by immunoblotting. Furthermore, the ubiquitination and cytoplasmic levels of
β
-catenin were assessed by immunoblotting, and also the localization of
β
-catenin was shown by green fluorescent protein-tagged
β
-catenin and time-lapse fluorescent imaging. Importantly, aspirin treatment caused increased phosphorylation of protein phosphatase 2A (PP2A), an event associated with inhibition of PP2A enzymatic activity, which was confirmed by a reduction in enzymatic PP2A activity. Moreover, this inhibition of PP2A enzymatic activity was essential for the effects of aspirin on the Wnt/
β
-catenin pathway as shown by transient transfection with PP2A constructs. The findings in this article provide a molecular explanation for the efficacy of aspirin in chemoprevention of colorectal cancer and shows biochemical evidence that PP2A is an important regulator of Wnt/
β
-catenin pathway activity in these cells.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>16878161</pmid><doi>10.1038/sj.onc.1209658</doi><tpages>10</tpages></addata></record> |
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| ispartof | Oncogene, 2006-10, Vol.25 (49), p.6447-6456 |
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| language | eng |
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| source | MEDLINE; Nature; EZB-FREE-00999 freely available EZB journals; Alma/SFX Local Collection |
| subjects | Anaphase-Promoting Complex-Cyclosome Anti-inflammatory agents Anti-Inflammatory Agents, Non-Steroidal - pharmacology Apoptosis Aspirin Aspirin - pharmacology beta Catenin - metabolism Biological and medical sciences Cell Biology Cell physiology Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes Chemopreventive agents Colon cancer Colorectal cancer Colorectal carcinoma Cytoplasm - metabolism Down-Regulation - drug effects Enzymatic activity Fundamental and applied biological sciences. Psychology Gastroenterology. Liver. Pancreas. Abdomen Gene expression Gene Expression Regulation, Neoplastic - drug effects Genes, Reporter - drug effects Green fluorescent protein HCT116 Cells Human Genetics Humans Immunoblotting Inflammation Internal Medicine Localization Medical sciences Medicine Medicine & Public Health Molecular and cellular biology Oncology original-article Phosphatase Phosphoprotein phosphatase Phosphoprotein Phosphatases - metabolism Phosphoprotein Phosphatases - physiology Phosphorylation Phosphorylation - drug effects Protein phosphatase Protein Phosphatase 2 Protein Processing, Post-Translational - drug effects Proteins Signal Transduction - drug effects Stomach. Duodenum. Small intestine. Colon. Rectum. Anus TCF Transcription Factors - metabolism Transfection Tumor cell lines Tumor Cells, Cultured Tumors Ubiquitin - metabolism Ubiquitin-Protein Ligase Complexes - genetics Ubiquitination Wnt protein Wnt Proteins - metabolism β-Catenin |
| title | Effect of aspirin on the Wnt/β-catenin pathway is mediated via protein phosphatase 2A |
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