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Cyclic AMP Promotes cAMP-responsive Element-binding Protein-dependent Induction of Cellular Inhibitor of Apoptosis Protein-2 and Suppresses Apoptosis of Colon Cancer Cells through ERK1/2 and p38 MAPK
We recently reported that cAMP suppresses apoptosis in colon cancer cells and induces cellular inhibitor of apoptosis protein-2 (c-IAP2) via a cAMP-responsive element (CRE), suggesting a mechanism for chemoprevention of colon cancer by non-steroidal anti-inflammatory drugs. In this study, we used T8...
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Published in: | The Journal of biological chemistry 2004-06, Vol.279 (25), p.26176-26183 |
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description | We recently reported that cAMP suppresses apoptosis in colon cancer cells and induces cellular inhibitor of apoptosis protein-2 (c-IAP2) via a cAMP-responsive element (CRE), suggesting a mechanism for chemoprevention of colon cancer by non-steroidal anti-inflammatory drugs. In this study, we used T84 human colon cancer cells to define the pathway by which increases in cAMP induce c-IAP2 expression. Treatment with several different cAMP agonists stimulated phosphorylation of CRE-binding protein (CREB) and activated expression of c-IAP2 in a CREB-dependent manner. Studies with pharmacological inhibitors revealed that cAMP-dependent phosphorylation of CREB required activation of ERK1/2 and p38 MAPK but was largely independent of protein kinase A. Immunoblots and transcriptional reporter assays using specific inhibitors, as well as expression of constitutively active forms of MEK1 and MKK3, showed that c-IAP2 induction by cAMP is regulated predominantly through ERK1/2 and p38 MAPK and suggested involvement of p90 ribosomal protein S6 kinase and mitogen and stress response kinase-1 as well. Consistent with those results, we found that cAMP-dependent suppression of apoptosis was blocked by treatment with inhibitors of ERK1/2 and p38 MAPK. We conclude that cAMP can induce c-IAP2 expression in colon cancer cells through CREB phosphorylation and CRE-dependent transcription in a manner that involves activation of ERK1/2 and p38 MAPK. These results emphasize that activation of kinases other than protein kinase A can mediate the actions of agents that increase cAMP, particularly in the regulation of CREB-dependent events. |
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In this study, we used T84 human colon cancer cells to define the pathway by which increases in cAMP induce c-IAP2 expression. Treatment with several different cAMP agonists stimulated phosphorylation of CRE-binding protein (CREB) and activated expression of c-IAP2 in a CREB-dependent manner. Studies with pharmacological inhibitors revealed that cAMP-dependent phosphorylation of CREB required activation of ERK1/2 and p38 MAPK but was largely independent of protein kinase A. Immunoblots and transcriptional reporter assays using specific inhibitors, as well as expression of constitutively active forms of MEK1 and MKK3, showed that c-IAP2 induction by cAMP is regulated predominantly through ERK1/2 and p38 MAPK and suggested involvement of p90 ribosomal protein S6 kinase and mitogen and stress response kinase-1 as well. Consistent with those results, we found that cAMP-dependent suppression of apoptosis was blocked by treatment with inhibitors of ERK1/2 and p38 MAPK. We conclude that cAMP can induce c-IAP2 expression in colon cancer cells through CREB phosphorylation and CRE-dependent transcription in a manner that involves activation of ERK1/2 and p38 MAPK. These results emphasize that activation of kinases other than protein kinase A can mediate the actions of agents that increase cAMP, particularly in the regulation of CREB-dependent events.</description><identifier>ISSN: 0021-9258</identifier><identifier>EISSN: 1083-351X</identifier><identifier>DOI: 10.1074/jbc.M313346200</identifier><identifier>PMID: 15078890</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Anti-Inflammatory Agents, Non-Steroidal - pharmacology ; Apoptosis ; Caspase 3 ; Caspases - metabolism ; Cell Line ; Cell Line, Tumor ; Colonic Neoplasms - pathology ; Cyclic AMP - metabolism ; Cyclic AMP Response Element-Binding Protein - metabolism ; Cyclic AMP-Dependent Protein Kinases - metabolism ; Enzyme Activation ; Enzyme Inhibitors - pharmacology ; Humans ; Immunoblotting ; Inhibitor of Apoptosis Proteins ; Luciferases - metabolism ; MAP Kinase Kinase 1 ; MAP Kinase Kinase 3 ; Mitogen-Activated Protein Kinase 1 - metabolism ; Mitogen-Activated Protein Kinase 3 ; Mitogen-Activated Protein Kinase Kinases - metabolism ; Mitogen-Activated Protein Kinases - metabolism ; Models, Biological ; p38 Mitogen-Activated Protein Kinases ; Phosphorylation ; Plasmids - metabolism ; Protein Binding ; Protein-Tyrosine Kinases - metabolism ; Proteins - metabolism ; Ribosomal Protein S6 Kinases, 90-kDa - metabolism ; Transcription, Genetic ; Transfection</subject><ispartof>The Journal of biological chemistry, 2004-06, Vol.279 (25), p.26176-26183</ispartof><rights>2004 © 2004 ASBMB. Currently published by Elsevier Inc; originally published by American Society for Biochemistry and Molecular Biology.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c409t-ac10c8cec714f3ff4274502657116292fe8dd39fb83efc1611ae2a6cf26a24a83</citedby><cites>FETCH-LOGICAL-c409t-ac10c8cec714f3ff4274502657116292fe8dd39fb83efc1611ae2a6cf26a24a83</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0021925820855963$$EHTML$$P50$$Gelsevier$$Hfree_for_read</linktohtml><link.rule.ids>314,780,784,3549,27924,27925,45780</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15078890$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Nishihara, Hiroshi</creatorcontrib><creatorcontrib>Hwang, Michael</creatorcontrib><creatorcontrib>Kizaka-Kondoh, Shinae</creatorcontrib><creatorcontrib>Eckmann, Lars</creatorcontrib><creatorcontrib>Insel, Paul A.</creatorcontrib><title>Cyclic AMP Promotes cAMP-responsive Element-binding Protein-dependent Induction of Cellular Inhibitor of Apoptosis Protein-2 and Suppresses Apoptosis of Colon Cancer Cells through ERK1/2 and p38 MAPK</title><title>The Journal of biological chemistry</title><addtitle>J Biol Chem</addtitle><description>We recently reported that cAMP suppresses apoptosis in colon cancer cells and induces cellular inhibitor of apoptosis protein-2 (c-IAP2) via a cAMP-responsive element (CRE), suggesting a mechanism for chemoprevention of colon cancer by non-steroidal anti-inflammatory drugs. In this study, we used T84 human colon cancer cells to define the pathway by which increases in cAMP induce c-IAP2 expression. Treatment with several different cAMP agonists stimulated phosphorylation of CRE-binding protein (CREB) and activated expression of c-IAP2 in a CREB-dependent manner. Studies with pharmacological inhibitors revealed that cAMP-dependent phosphorylation of CREB required activation of ERK1/2 and p38 MAPK but was largely independent of protein kinase A. Immunoblots and transcriptional reporter assays using specific inhibitors, as well as expression of constitutively active forms of MEK1 and MKK3, showed that c-IAP2 induction by cAMP is regulated predominantly through ERK1/2 and p38 MAPK and suggested involvement of p90 ribosomal protein S6 kinase and mitogen and stress response kinase-1 as well. Consistent with those results, we found that cAMP-dependent suppression of apoptosis was blocked by treatment with inhibitors of ERK1/2 and p38 MAPK. We conclude that cAMP can induce c-IAP2 expression in colon cancer cells through CREB phosphorylation and CRE-dependent transcription in a manner that involves activation of ERK1/2 and p38 MAPK. These results emphasize that activation of kinases other than protein kinase A can mediate the actions of agents that increase cAMP, particularly in the regulation of CREB-dependent events.</description><subject>Anti-Inflammatory Agents, Non-Steroidal - pharmacology</subject><subject>Apoptosis</subject><subject>Caspase 3</subject><subject>Caspases - metabolism</subject><subject>Cell Line</subject><subject>Cell Line, Tumor</subject><subject>Colonic Neoplasms - pathology</subject><subject>Cyclic AMP - metabolism</subject><subject>Cyclic AMP Response Element-Binding Protein - metabolism</subject><subject>Cyclic AMP-Dependent Protein Kinases - metabolism</subject><subject>Enzyme Activation</subject><subject>Enzyme Inhibitors - pharmacology</subject><subject>Humans</subject><subject>Immunoblotting</subject><subject>Inhibitor of Apoptosis Proteins</subject><subject>Luciferases - metabolism</subject><subject>MAP Kinase Kinase 1</subject><subject>MAP Kinase Kinase 3</subject><subject>Mitogen-Activated Protein Kinase 1 - metabolism</subject><subject>Mitogen-Activated Protein Kinase 3</subject><subject>Mitogen-Activated Protein Kinase Kinases - metabolism</subject><subject>Mitogen-Activated Protein Kinases - metabolism</subject><subject>Models, Biological</subject><subject>p38 Mitogen-Activated Protein Kinases</subject><subject>Phosphorylation</subject><subject>Plasmids - metabolism</subject><subject>Protein Binding</subject><subject>Protein-Tyrosine Kinases - metabolism</subject><subject>Proteins - metabolism</subject><subject>Ribosomal Protein S6 Kinases, 90-kDa - metabolism</subject><subject>Transcription, Genetic</subject><subject>Transfection</subject><issn>0021-9258</issn><issn>1083-351X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><recordid>eNp1kUuP0zAUhS0EYkphyxJ5gdil40eeyyrqwGimouIhsbMc-6bxKLGDnQyaX8jfwiUVXeGN5evvnHt1D0JvKdlQUqTXD43a7DnlPM0ZIc_QipKSJzyjP56jFSGMJhXLyiv0KoQHEk9a0ZfoimakKMuKrNDv-kn1RuHt_oAP3g1ugoBVfCUewuhsMI-Adz0MYKekMVYbezyBExibaBjB6viDb62e1WScxa7FNfT93Esfq51pzOT8qbod3Ti5YMI_OcPSavx1HsfYK8S-F-Tk4vpoV0urwP-1DHjqvJuPHd59uaPXi3rkJd5vD3ev0YtW9gHenO81-n6z-1Z_Su4_f7ytt_eJSkk1JVJRokoFqqBpy9s2ZUWaEZZnBaU5q1gLpda8apuSQ6toTqkEJnPVslyyVJZ8jT4svqN3P2cIkxhMUHE6acHNQRSM0CqPgazRZgGVdyF4aMXozSD9k6BEnKITMTpxiS4K3p2d52YAfcHPWUXg_QJ05tj9Mh5EY5zqYBCsqATLBMtpkUesXDCIa3g04EVQBuIWdZSoSWhn_jfCH_emtTA</recordid><startdate>20040618</startdate><enddate>20040618</enddate><creator>Nishihara, Hiroshi</creator><creator>Hwang, Michael</creator><creator>Kizaka-Kondoh, Shinae</creator><creator>Eckmann, Lars</creator><creator>Insel, Paul A.</creator><general>Elsevier Inc</general><general>American Society for Biochemistry and Molecular Biology</general><scope>6I.</scope><scope>AAFTH</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>7X8</scope></search><sort><creationdate>20040618</creationdate><title>Cyclic AMP Promotes cAMP-responsive Element-binding Protein-dependent Induction of Cellular Inhibitor of Apoptosis Protein-2 and Suppresses Apoptosis of Colon Cancer Cells through ERK1/2 and p38 MAPK</title><author>Nishihara, Hiroshi ; Hwang, Michael ; Kizaka-Kondoh, Shinae ; Eckmann, Lars ; Insel, Paul A.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c409t-ac10c8cec714f3ff4274502657116292fe8dd39fb83efc1611ae2a6cf26a24a83</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>Anti-Inflammatory Agents, Non-Steroidal - pharmacology</topic><topic>Apoptosis</topic><topic>Caspase 3</topic><topic>Caspases - metabolism</topic><topic>Cell Line</topic><topic>Cell Line, Tumor</topic><topic>Colonic Neoplasms - pathology</topic><topic>Cyclic AMP - metabolism</topic><topic>Cyclic AMP Response Element-Binding Protein - metabolism</topic><topic>Cyclic AMP-Dependent Protein Kinases - metabolism</topic><topic>Enzyme Activation</topic><topic>Enzyme Inhibitors - pharmacology</topic><topic>Humans</topic><topic>Immunoblotting</topic><topic>Inhibitor of Apoptosis Proteins</topic><topic>Luciferases - metabolism</topic><topic>MAP Kinase Kinase 1</topic><topic>MAP Kinase Kinase 3</topic><topic>Mitogen-Activated Protein Kinase 1 - metabolism</topic><topic>Mitogen-Activated Protein Kinase 3</topic><topic>Mitogen-Activated Protein Kinase Kinases - metabolism</topic><topic>Mitogen-Activated Protein Kinases - metabolism</topic><topic>Models, Biological</topic><topic>p38 Mitogen-Activated Protein Kinases</topic><topic>Phosphorylation</topic><topic>Plasmids - metabolism</topic><topic>Protein Binding</topic><topic>Protein-Tyrosine Kinases - metabolism</topic><topic>Proteins - metabolism</topic><topic>Ribosomal Protein S6 Kinases, 90-kDa - metabolism</topic><topic>Transcription, Genetic</topic><topic>Transfection</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Nishihara, Hiroshi</creatorcontrib><creatorcontrib>Hwang, Michael</creatorcontrib><creatorcontrib>Kizaka-Kondoh, Shinae</creatorcontrib><creatorcontrib>Eckmann, Lars</creatorcontrib><creatorcontrib>Insel, Paul A.</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><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>The Journal of biological chemistry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Nishihara, Hiroshi</au><au>Hwang, Michael</au><au>Kizaka-Kondoh, Shinae</au><au>Eckmann, Lars</au><au>Insel, Paul A.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Cyclic AMP Promotes cAMP-responsive Element-binding Protein-dependent Induction of Cellular Inhibitor of Apoptosis Protein-2 and Suppresses Apoptosis of Colon Cancer Cells through ERK1/2 and p38 MAPK</atitle><jtitle>The Journal of biological chemistry</jtitle><addtitle>J Biol Chem</addtitle><date>2004-06-18</date><risdate>2004</risdate><volume>279</volume><issue>25</issue><spage>26176</spage><epage>26183</epage><pages>26176-26183</pages><issn>0021-9258</issn><eissn>1083-351X</eissn><abstract>We recently reported that cAMP suppresses apoptosis in colon cancer cells and induces cellular inhibitor of apoptosis protein-2 (c-IAP2) via a cAMP-responsive element (CRE), suggesting a mechanism for chemoprevention of colon cancer by non-steroidal anti-inflammatory drugs. In this study, we used T84 human colon cancer cells to define the pathway by which increases in cAMP induce c-IAP2 expression. Treatment with several different cAMP agonists stimulated phosphorylation of CRE-binding protein (CREB) and activated expression of c-IAP2 in a CREB-dependent manner. Studies with pharmacological inhibitors revealed that cAMP-dependent phosphorylation of CREB required activation of ERK1/2 and p38 MAPK but was largely independent of protein kinase A. Immunoblots and transcriptional reporter assays using specific inhibitors, as well as expression of constitutively active forms of MEK1 and MKK3, showed that c-IAP2 induction by cAMP is regulated predominantly through ERK1/2 and p38 MAPK and suggested involvement of p90 ribosomal protein S6 kinase and mitogen and stress response kinase-1 as well. Consistent with those results, we found that cAMP-dependent suppression of apoptosis was blocked by treatment with inhibitors of ERK1/2 and p38 MAPK. We conclude that cAMP can induce c-IAP2 expression in colon cancer cells through CREB phosphorylation and CRE-dependent transcription in a manner that involves activation of ERK1/2 and p38 MAPK. These results emphasize that activation of kinases other than protein kinase A can mediate the actions of agents that increase cAMP, particularly in the regulation of CREB-dependent events.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>15078890</pmid><doi>10.1074/jbc.M313346200</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Anti-Inflammatory Agents, Non-Steroidal - pharmacology Apoptosis Caspase 3 Caspases - metabolism Cell Line Cell Line, Tumor Colonic Neoplasms - pathology Cyclic AMP - metabolism Cyclic AMP Response Element-Binding Protein - metabolism Cyclic AMP-Dependent Protein Kinases - metabolism Enzyme Activation Enzyme Inhibitors - pharmacology Humans Immunoblotting Inhibitor of Apoptosis Proteins Luciferases - metabolism MAP Kinase Kinase 1 MAP Kinase Kinase 3 Mitogen-Activated Protein Kinase 1 - metabolism Mitogen-Activated Protein Kinase 3 Mitogen-Activated Protein Kinase Kinases - metabolism Mitogen-Activated Protein Kinases - metabolism Models, Biological p38 Mitogen-Activated Protein Kinases Phosphorylation Plasmids - metabolism Protein Binding Protein-Tyrosine Kinases - metabolism Proteins - metabolism Ribosomal Protein S6 Kinases, 90-kDa - metabolism Transcription, Genetic Transfection |
title | Cyclic AMP Promotes cAMP-responsive Element-binding Protein-dependent Induction of Cellular Inhibitor of Apoptosis Protein-2 and Suppresses Apoptosis of Colon Cancer Cells through ERK1/2 and p38 MAPK |
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