MAPK-ERK activation in kidney of male rats chronically fed ochratoxin A at a dose causing a significant incidence of renal carcinoma
Kidney samples of male Fischer 344 (F-344) rats fed a carcinogenic dose of OTA over 7 days, 21 days and 12 months were analysed for various cell signalling proteins known to be potentially involved in chemical carcinogenicity. OTA was found to increase the phosphorylation of atypical-PKC. This was c...
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| creator | Marin-Kuan, M. Nestler, S. Verguet, C. Bezençon, C. Piguet, D. Delatour, T. Mantle, P. Cavin, C. Schilter, B. |
| description | Kidney samples of male Fischer 344 (F-344) rats fed a carcinogenic dose of OTA over 7 days, 21 days and 12 months were analysed for various cell signalling proteins known to be potentially involved in chemical carcinogenicity. OTA was found to increase the phosphorylation of atypical-PKC. This was correlated with a selective downstream activation of the MAP-kinase extracellular regulated kinases isoforms 1 and 2 (ERK1/2) and of their substrates ELK1/2 and p90RSK. Moreover, analysis of effectors acting upstream of PKC indicated a possible mobilisation of the insulin-like growth factor-1 receptor (lGFr) and phosphoinositide-dependent kinase-1 (PDK1) system. An increased histone deacetylase (HDAC) enzymatic activity associated with enhanced HDAC3 protein expression was also observed. These findings are potentially relevant with respect to the understanding of OTA nephrocarcinogenicity. HDAC-induced gene silencing has previously been shown to play a role in tumour development. Furthermore, PKC and the MEK-ERK MAP-kinase pathways are known to play important roles in cell proliferation, cell survival, anti-apoptotic activity and renal cancer development. |
| doi_str_mv | 10.1016/j.taap.2007.06.014 |
| format | Article |
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OTA was found to increase the phosphorylation of atypical-PKC. This was correlated with a selective downstream activation of the MAP-kinase extracellular regulated kinases isoforms 1 and 2 (ERK1/2) and of their substrates ELK1/2 and p90RSK. Moreover, analysis of effectors acting upstream of PKC indicated a possible mobilisation of the insulin-like growth factor-1 receptor (lGFr) and phosphoinositide-dependent kinase-1 (PDK1) system. An increased histone deacetylase (HDAC) enzymatic activity associated with enhanced HDAC3 protein expression was also observed. These findings are potentially relevant with respect to the understanding of OTA nephrocarcinogenicity. HDAC-induced gene silencing has previously been shown to play a role in tumour development. Furthermore, PKC and the MEK-ERK MAP-kinase pathways are known to play important roles in cell proliferation, cell survival, anti-apoptotic activity and renal cancer development.</description><identifier>ISSN: 0041-008X</identifier><identifier>EISSN: 1096-0333</identifier><identifier>DOI: 10.1016/j.taap.2007.06.014</identifier><identifier>PMID: 17651772</identifier><identifier>CODEN: TXAPA9</identifier><language>eng</language><publisher>San Diego, CA: Elsevier Inc</publisher><subject>3-Phosphoinositide-Dependent Protein Kinases ; 60 APPLIED LIFE SCIENCES ; Animals ; Biological and medical sciences ; Blotting, Western ; Carcinogens - administration & dosage ; Carcinogens - toxicity ; CARCINOMAS ; CELL PROLIFERATION ; Cell signalling ; DOSES ; ets-Domain Protein Elk-1 - drug effects ; ets-Domain Protein Elk-1 - metabolism ; Gene Expression Regulation - drug effects ; GROWTH FACTORS ; Histone Deacetylases - metabolism ; INSULIN ; Kidney - metabolism ; Kidney Neoplasms - chemically induced ; Kidney Neoplasms - physiopathology ; KIDNEYS ; Male ; MAP Kinase Signaling System - drug effects ; MAP kinases ; Medical sciences ; Mitogen-Activated Protein Kinase 1 - drug effects ; Mitogen-Activated Protein Kinase 1 - metabolism ; Mitogen-Activated Protein Kinase 3 - drug effects ; Mitogen-Activated Protein Kinase 3 - metabolism ; Nephrocarcinogenicity ; Nephrology. Urinary tract diseases ; Ochratoxin A ; Ochratoxins - administration & dosage ; Ochratoxins - toxicity ; PHOSPHORYLATION ; PHOSPHOTRANSFERASES ; PKC-ζ ; Plant poisons toxicology ; Protein-Serine-Threonine Kinases - drug effects ; Protein-Serine-Threonine Kinases - metabolism ; RATS ; Rats, Inbred F344 ; Receptor, IGF Type 1 - drug effects ; Receptor, IGF Type 1 - metabolism ; RECEPTORS ; Ribosomal Protein S6 Kinases, 90-kDa - drug effects ; Ribosomal Protein S6 Kinases, 90-kDa - metabolism ; Time Factors ; Toxicology ; Tumors of the urinary system</subject><ispartof>Toxicology and applied pharmacology, 2007-10, Vol.224 (2), p.174-181</ispartof><rights>2007 Elsevier Inc.</rights><rights>2007 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c509t-d0aaf2d717c22661887ef4d2d7d3e6717024c6c13602481f80f376464f5c7ed53</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.taap.2007.06.014$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>230,314,780,784,885,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=19163431$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17651772$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://www.osti.gov/biblio/21077825$$D View this record in Osti.gov$$Hfree_for_read</backlink></links><search><creatorcontrib>Marin-Kuan, M.</creatorcontrib><creatorcontrib>Nestler, S.</creatorcontrib><creatorcontrib>Verguet, C.</creatorcontrib><creatorcontrib>Bezençon, C.</creatorcontrib><creatorcontrib>Piguet, D.</creatorcontrib><creatorcontrib>Delatour, T.</creatorcontrib><creatorcontrib>Mantle, P.</creatorcontrib><creatorcontrib>Cavin, C.</creatorcontrib><creatorcontrib>Schilter, B.</creatorcontrib><title>MAPK-ERK activation in kidney of male rats chronically fed ochratoxin A at a dose causing a significant incidence of renal carcinoma</title><title>Toxicology and applied pharmacology</title><addtitle>Toxicol Appl Pharmacol</addtitle><description>Kidney samples of male Fischer 344 (F-344) rats fed a carcinogenic dose of OTA over 7 days, 21 days and 12 months were analysed for various cell signalling proteins known to be potentially involved in chemical carcinogenicity. OTA was found to increase the phosphorylation of atypical-PKC. This was correlated with a selective downstream activation of the MAP-kinase extracellular regulated kinases isoforms 1 and 2 (ERK1/2) and of their substrates ELK1/2 and p90RSK. Moreover, analysis of effectors acting upstream of PKC indicated a possible mobilisation of the insulin-like growth factor-1 receptor (lGFr) and phosphoinositide-dependent kinase-1 (PDK1) system. An increased histone deacetylase (HDAC) enzymatic activity associated with enhanced HDAC3 protein expression was also observed. These findings are potentially relevant with respect to the understanding of OTA nephrocarcinogenicity. HDAC-induced gene silencing has previously been shown to play a role in tumour development. Furthermore, PKC and the MEK-ERK MAP-kinase pathways are known to play important roles in cell proliferation, cell survival, anti-apoptotic activity and renal cancer development.</description><subject>3-Phosphoinositide-Dependent Protein Kinases</subject><subject>60 APPLIED LIFE SCIENCES</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Blotting, Western</subject><subject>Carcinogens - administration & dosage</subject><subject>Carcinogens - toxicity</subject><subject>CARCINOMAS</subject><subject>CELL PROLIFERATION</subject><subject>Cell signalling</subject><subject>DOSES</subject><subject>ets-Domain Protein Elk-1 - drug effects</subject><subject>ets-Domain Protein Elk-1 - metabolism</subject><subject>Gene Expression Regulation - drug effects</subject><subject>GROWTH FACTORS</subject><subject>Histone Deacetylases - metabolism</subject><subject>INSULIN</subject><subject>Kidney - metabolism</subject><subject>Kidney Neoplasms - chemically induced</subject><subject>Kidney Neoplasms - physiopathology</subject><subject>KIDNEYS</subject><subject>Male</subject><subject>MAP Kinase Signaling System - drug effects</subject><subject>MAP kinases</subject><subject>Medical sciences</subject><subject>Mitogen-Activated Protein Kinase 1 - drug effects</subject><subject>Mitogen-Activated Protein Kinase 1 - metabolism</subject><subject>Mitogen-Activated Protein Kinase 3 - drug effects</subject><subject>Mitogen-Activated Protein Kinase 3 - metabolism</subject><subject>Nephrocarcinogenicity</subject><subject>Nephrology. Urinary tract diseases</subject><subject>Ochratoxin A</subject><subject>Ochratoxins - administration & dosage</subject><subject>Ochratoxins - toxicity</subject><subject>PHOSPHORYLATION</subject><subject>PHOSPHOTRANSFERASES</subject><subject>PKC-ζ</subject><subject>Plant poisons toxicology</subject><subject>Protein-Serine-Threonine Kinases - drug effects</subject><subject>Protein-Serine-Threonine Kinases - metabolism</subject><subject>RATS</subject><subject>Rats, Inbred F344</subject><subject>Receptor, IGF Type 1 - drug effects</subject><subject>Receptor, IGF Type 1 - metabolism</subject><subject>RECEPTORS</subject><subject>Ribosomal Protein S6 Kinases, 90-kDa - drug effects</subject><subject>Ribosomal Protein S6 Kinases, 90-kDa - metabolism</subject><subject>Time Factors</subject><subject>Toxicology</subject><subject>Tumors of the urinary system</subject><issn>0041-008X</issn><issn>1096-0333</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kc2KFDEUhYMoTjv6Ai4kILqr8iZVnVSBm2YYf5gRRRTchZjczKStStokPdh7H9wU3TA7V0kO3z3knkPIcwYtAybebNui9a7lALIF0QLrH5AVg1E00HXdQ7IC6FkDMPw4I09y3gLA2PfsMTljUqyZlHxF_n7afLlqLr9eUW2Kv9PFx0B9oL-8DXig0dFZT0iTLpma2xSDN3qaDtShpbEKusQ_Fd9QXaimNmakRu-zDzf1mf1N8K5OhFI9jbcYDC6eCYOeKpiMD3HWT8kjp6eMz07nOfn-7vLbxYfm-vP7jxeb68asYSyNBa0dt5JJw7kQbBgkut5WxXYoqgy8N8KwTtTLwNwArpOiF71bG4l23Z2Tl0ffmItX2fiC5tbEENAUxRlIOfCFen2kdin-3mMuavbZ4DTpgHGfFRuHgYMYK8iPoEkx54RO7ZKfdTooBmppSG3V0pBaGlIgVG2oDr04ue9_zmjvR06VVODVCdC5Zu2Srsnle25kous7Vrm3Rw5rYnce07LQErD1adnHRv-_f_wDZkyuFw</recordid><startdate>20071015</startdate><enddate>20071015</enddate><creator>Marin-Kuan, M.</creator><creator>Nestler, S.</creator><creator>Verguet, C.</creator><creator>Bezençon, C.</creator><creator>Piguet, D.</creator><creator>Delatour, T.</creator><creator>Mantle, P.</creator><creator>Cavin, C.</creator><creator>Schilter, B.</creator><general>Elsevier Inc</general><general>Elsevier</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>7TM</scope><scope>7U7</scope><scope>C1K</scope><scope>OTOTI</scope></search><sort><creationdate>20071015</creationdate><title>MAPK-ERK activation in kidney of male rats chronically fed ochratoxin A at a dose causing a significant incidence of renal carcinoma</title><author>Marin-Kuan, M. ; Nestler, S. ; Verguet, C. ; Bezençon, C. ; Piguet, D. ; Delatour, T. ; Mantle, P. ; Cavin, C. ; Schilter, B.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c509t-d0aaf2d717c22661887ef4d2d7d3e6717024c6c13602481f80f376464f5c7ed53</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2007</creationdate><topic>3-Phosphoinositide-Dependent Protein Kinases</topic><topic>60 APPLIED LIFE SCIENCES</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Blotting, Western</topic><topic>Carcinogens - administration & dosage</topic><topic>Carcinogens - toxicity</topic><topic>CARCINOMAS</topic><topic>CELL PROLIFERATION</topic><topic>Cell signalling</topic><topic>DOSES</topic><topic>ets-Domain Protein Elk-1 - drug effects</topic><topic>ets-Domain Protein Elk-1 - metabolism</topic><topic>Gene Expression Regulation - drug effects</topic><topic>GROWTH FACTORS</topic><topic>Histone Deacetylases - metabolism</topic><topic>INSULIN</topic><topic>Kidney - metabolism</topic><topic>Kidney Neoplasms - chemically induced</topic><topic>Kidney Neoplasms - physiopathology</topic><topic>KIDNEYS</topic><topic>Male</topic><topic>MAP Kinase Signaling System - drug effects</topic><topic>MAP kinases</topic><topic>Medical sciences</topic><topic>Mitogen-Activated Protein Kinase 1 - drug effects</topic><topic>Mitogen-Activated Protein Kinase 1 - metabolism</topic><topic>Mitogen-Activated Protein Kinase 3 - drug effects</topic><topic>Mitogen-Activated Protein Kinase 3 - metabolism</topic><topic>Nephrocarcinogenicity</topic><topic>Nephrology. Urinary tract diseases</topic><topic>Ochratoxin A</topic><topic>Ochratoxins - administration & dosage</topic><topic>Ochratoxins - toxicity</topic><topic>PHOSPHORYLATION</topic><topic>PHOSPHOTRANSFERASES</topic><topic>PKC-ζ</topic><topic>Plant poisons toxicology</topic><topic>Protein-Serine-Threonine Kinases - drug effects</topic><topic>Protein-Serine-Threonine Kinases - metabolism</topic><topic>RATS</topic><topic>Rats, Inbred F344</topic><topic>Receptor, IGF Type 1 - drug effects</topic><topic>Receptor, IGF Type 1 - metabolism</topic><topic>RECEPTORS</topic><topic>Ribosomal Protein S6 Kinases, 90-kDa - drug effects</topic><topic>Ribosomal Protein S6 Kinases, 90-kDa - metabolism</topic><topic>Time Factors</topic><topic>Toxicology</topic><topic>Tumors of the urinary system</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Marin-Kuan, M.</creatorcontrib><creatorcontrib>Nestler, S.</creatorcontrib><creatorcontrib>Verguet, C.</creatorcontrib><creatorcontrib>Bezençon, C.</creatorcontrib><creatorcontrib>Piguet, D.</creatorcontrib><creatorcontrib>Delatour, T.</creatorcontrib><creatorcontrib>Mantle, P.</creatorcontrib><creatorcontrib>Cavin, C.</creatorcontrib><creatorcontrib>Schilter, B.</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>Nucleic Acids Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><collection>OSTI.GOV</collection><jtitle>Toxicology and applied pharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Marin-Kuan, M.</au><au>Nestler, S.</au><au>Verguet, C.</au><au>Bezençon, C.</au><au>Piguet, D.</au><au>Delatour, T.</au><au>Mantle, P.</au><au>Cavin, C.</au><au>Schilter, B.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>MAPK-ERK activation in kidney of male rats chronically fed ochratoxin A at a dose causing a significant incidence of renal carcinoma</atitle><jtitle>Toxicology and applied pharmacology</jtitle><addtitle>Toxicol Appl Pharmacol</addtitle><date>2007-10-15</date><risdate>2007</risdate><volume>224</volume><issue>2</issue><spage>174</spage><epage>181</epage><pages>174-181</pages><issn>0041-008X</issn><eissn>1096-0333</eissn><coden>TXAPA9</coden><abstract>Kidney samples of male Fischer 344 (F-344) rats fed a carcinogenic dose of OTA over 7 days, 21 days and 12 months were analysed for various cell signalling proteins known to be potentially involved in chemical carcinogenicity. OTA was found to increase the phosphorylation of atypical-PKC. This was correlated with a selective downstream activation of the MAP-kinase extracellular regulated kinases isoforms 1 and 2 (ERK1/2) and of their substrates ELK1/2 and p90RSK. Moreover, analysis of effectors acting upstream of PKC indicated a possible mobilisation of the insulin-like growth factor-1 receptor (lGFr) and phosphoinositide-dependent kinase-1 (PDK1) system. An increased histone deacetylase (HDAC) enzymatic activity associated with enhanced HDAC3 protein expression was also observed. These findings are potentially relevant with respect to the understanding of OTA nephrocarcinogenicity. HDAC-induced gene silencing has previously been shown to play a role in tumour development. Furthermore, PKC and the MEK-ERK MAP-kinase pathways are known to play important roles in cell proliferation, cell survival, anti-apoptotic activity and renal cancer development.</abstract><cop>San Diego, CA</cop><pub>Elsevier Inc</pub><pmid>17651772</pmid><doi>10.1016/j.taap.2007.06.014</doi><tpages>8</tpages></addata></record> |
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| ispartof | Toxicology and applied pharmacology, 2007-10, Vol.224 (2), p.174-181 |
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| language | eng |
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| source | MEDLINE; ScienceDirect Journals (5 years ago - present) |
| subjects | 3-Phosphoinositide-Dependent Protein Kinases 60 APPLIED LIFE SCIENCES Animals Biological and medical sciences Blotting, Western Carcinogens - administration & dosage Carcinogens - toxicity CARCINOMAS CELL PROLIFERATION Cell signalling DOSES ets-Domain Protein Elk-1 - drug effects ets-Domain Protein Elk-1 - metabolism Gene Expression Regulation - drug effects GROWTH FACTORS Histone Deacetylases - metabolism INSULIN Kidney - metabolism Kidney Neoplasms - chemically induced Kidney Neoplasms - physiopathology KIDNEYS Male MAP Kinase Signaling System - drug effects MAP kinases Medical sciences Mitogen-Activated Protein Kinase 1 - drug effects Mitogen-Activated Protein Kinase 1 - metabolism Mitogen-Activated Protein Kinase 3 - drug effects Mitogen-Activated Protein Kinase 3 - metabolism Nephrocarcinogenicity Nephrology. Urinary tract diseases Ochratoxin A Ochratoxins - administration & dosage Ochratoxins - toxicity PHOSPHORYLATION PHOSPHOTRANSFERASES PKC-ζ Plant poisons toxicology Protein-Serine-Threonine Kinases - drug effects Protein-Serine-Threonine Kinases - metabolism RATS Rats, Inbred F344 Receptor, IGF Type 1 - drug effects Receptor, IGF Type 1 - metabolism RECEPTORS Ribosomal Protein S6 Kinases, 90-kDa - drug effects Ribosomal Protein S6 Kinases, 90-kDa - metabolism Time Factors Toxicology Tumors of the urinary system |
| title | MAPK-ERK activation in kidney of male rats chronically fed ochratoxin A at a dose causing a significant incidence of renal carcinoma |
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