Increased Expression of Insulin Receptor Substrate-1 in Human Pancreatic Cancer
Insulin receptor substrate-1 (IRS-1) is a multisite docking protein implicated in mitogenic signaling following activation of the insulin and insulin-like growth factor I receptors. In the present study we characterized IRS-1 expression in human pancreatic cancer. Northern blot analysis revealed hig...
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Veröffentlicht in: | Biochemical and biophysical research communications 1996-03, Vol.220 (3), p.886-890 |
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creator | Bergmann, Uwe Funatomi, Hitoshi Kornmann, Marko Beger, Hans G. Korc, Murray |
description | Insulin receptor substrate-1 (IRS-1) is a multisite docking protein implicated in mitogenic signaling following activation of the insulin and insulin-like growth factor I receptors. In the present study we characterized IRS-1 expression in human pancreatic cancer. Northern blot analysis revealed high levels of IRS-1 mRNA transcripts in ASPC-1 and MIA PaCa-2 human pancreatic cancer cell lines, and lower levels in COLO-357, PANC-1, and T3M4 cells. Immunoblotting with anti-IRS-1 antibodies indicated that IRS-1 protein levels paralleled IRS-1 mRNA levels. Analysis of RNA isolated from normal and cancerous human pancreatic tissues indicated that 7 of 16 pancreatic cancer samples overexpressed IRS-1 mRNA transcripts by comparison with the normal pancreas and that insulin mRNA levels were abundant in many tumors. These data suggest that IRS-1 contributes to the signaling pathways that lead to excessive growth stimulation in human pancreatic cancer. |
doi_str_mv | 10.1006/bbrc.1996.0500 |
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In the present study we characterized IRS-1 expression in human pancreatic cancer. Northern blot analysis revealed high levels of IRS-1 mRNA transcripts in ASPC-1 and MIA PaCa-2 human pancreatic cancer cell lines, and lower levels in COLO-357, PANC-1, and T3M4 cells. Immunoblotting with anti-IRS-1 antibodies indicated that IRS-1 protein levels paralleled IRS-1 mRNA levels. Analysis of RNA isolated from normal and cancerous human pancreatic tissues indicated that 7 of 16 pancreatic cancer samples overexpressed IRS-1 mRNA transcripts by comparison with the normal pancreas and that insulin mRNA levels were abundant in many tumors. These data suggest that IRS-1 contributes to the signaling pathways that lead to excessive growth stimulation in human pancreatic cancer.</description><identifier>ISSN: 0006-291X</identifier><identifier>EISSN: 1090-2104</identifier><identifier>DOI: 10.1006/bbrc.1996.0500</identifier><identifier>PMID: 8607861</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Blotting, Northern ; Cell Line ; Colonic Neoplasms ; Gene Expression - drug effects ; Humans ; Insulin - biosynthesis ; Insulin - pharmacology ; Insulin Receptor Substrate Proteins ; Pancreas - metabolism ; Pancreatic Neoplasms - metabolism ; Phosphoproteins - biosynthesis ; Phosphoproteins - isolation & purification ; RNA, Messenger - analysis ; RNA, Messenger - biosynthesis ; Transcription, Genetic ; Tumor Cells, Cultured</subject><ispartof>Biochemical and biophysical research communications, 1996-03, Vol.220 (3), p.886-890</ispartof><rights>1996 Academic Press</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c405t-e3fcb77a602f5a4f38a45fb30bc1beb04c20d5a490284314b3cc55152fd0eeeb3</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1006/bbrc.1996.0500$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/8607861$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Bergmann, Uwe</creatorcontrib><creatorcontrib>Funatomi, Hitoshi</creatorcontrib><creatorcontrib>Kornmann, Marko</creatorcontrib><creatorcontrib>Beger, Hans G.</creatorcontrib><creatorcontrib>Korc, Murray</creatorcontrib><title>Increased Expression of Insulin Receptor Substrate-1 in Human Pancreatic Cancer</title><title>Biochemical and biophysical research communications</title><addtitle>Biochem Biophys Res Commun</addtitle><description>Insulin receptor substrate-1 (IRS-1) is a multisite docking protein implicated in mitogenic signaling following activation of the insulin and insulin-like growth factor I receptors. In the present study we characterized IRS-1 expression in human pancreatic cancer. Northern blot analysis revealed high levels of IRS-1 mRNA transcripts in ASPC-1 and MIA PaCa-2 human pancreatic cancer cell lines, and lower levels in COLO-357, PANC-1, and T3M4 cells. Immunoblotting with anti-IRS-1 antibodies indicated that IRS-1 protein levels paralleled IRS-1 mRNA levels. Analysis of RNA isolated from normal and cancerous human pancreatic tissues indicated that 7 of 16 pancreatic cancer samples overexpressed IRS-1 mRNA transcripts by comparison with the normal pancreas and that insulin mRNA levels were abundant in many tumors. These data suggest that IRS-1 contributes to the signaling pathways that lead to excessive growth stimulation in human pancreatic cancer.</description><subject>Blotting, Northern</subject><subject>Cell Line</subject><subject>Colonic Neoplasms</subject><subject>Gene Expression - drug effects</subject><subject>Humans</subject><subject>Insulin - biosynthesis</subject><subject>Insulin - pharmacology</subject><subject>Insulin Receptor Substrate Proteins</subject><subject>Pancreas - metabolism</subject><subject>Pancreatic Neoplasms - metabolism</subject><subject>Phosphoproteins - biosynthesis</subject><subject>Phosphoproteins - isolation & purification</subject><subject>RNA, Messenger - analysis</subject><subject>RNA, Messenger - biosynthesis</subject><subject>Transcription, Genetic</subject><subject>Tumor Cells, Cultured</subject><issn>0006-291X</issn><issn>1090-2104</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1996</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kM1LAzEQxYMotVav3oScvG2d7Cb7cZSitlCo-AHeQpKdhch-meyK_vdmbfHmaYZ5bx68HyGXDJYMIL3R2pklK4p0CQLgiMwZFBDFDPgxmUNwRHHB3k7JmffvAIzxtJiRWZ5ClqdsTnab1jhUHkt699U79N52Le0qumn9WNuWPqHBfugcfR61H5waMGI03Ndjo1r6qH7fB2voKqzozslJpWqPF4e5IK_3dy-rdbTdPWxWt9vIcBBDhElldJapFOJKKF4lueKi0glowzRq4CaGMggFxDlPGNeJMUIwEVclIKJOFuR6n9u77mNEP8jGeoN1rVrsRi-zrChyIdJgXO6NxnXeO6xk72yj3LdkICeCciIoJ4JyIhgerg7Jo26w_LMfkAU93-sY6n1adNIbi6F7aR2aQZad_S_6B0Ytf-U</recordid><startdate>19960327</startdate><enddate>19960327</enddate><creator>Bergmann, Uwe</creator><creator>Funatomi, Hitoshi</creator><creator>Kornmann, Marko</creator><creator>Beger, Hans G.</creator><creator>Korc, Murray</creator><general>Elsevier Inc</general><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>19960327</creationdate><title>Increased Expression of Insulin Receptor Substrate-1 in Human Pancreatic Cancer</title><author>Bergmann, Uwe ; Funatomi, Hitoshi ; Kornmann, Marko ; Beger, Hans G. ; Korc, Murray</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c405t-e3fcb77a602f5a4f38a45fb30bc1beb04c20d5a490284314b3cc55152fd0eeeb3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1996</creationdate><topic>Blotting, Northern</topic><topic>Cell Line</topic><topic>Colonic Neoplasms</topic><topic>Gene Expression - drug effects</topic><topic>Humans</topic><topic>Insulin - biosynthesis</topic><topic>Insulin - pharmacology</topic><topic>Insulin Receptor Substrate Proteins</topic><topic>Pancreas - metabolism</topic><topic>Pancreatic Neoplasms - metabolism</topic><topic>Phosphoproteins - biosynthesis</topic><topic>Phosphoproteins - isolation & purification</topic><topic>RNA, Messenger - analysis</topic><topic>RNA, Messenger - biosynthesis</topic><topic>Transcription, Genetic</topic><topic>Tumor Cells, Cultured</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Bergmann, Uwe</creatorcontrib><creatorcontrib>Funatomi, Hitoshi</creatorcontrib><creatorcontrib>Kornmann, Marko</creatorcontrib><creatorcontrib>Beger, Hans G.</creatorcontrib><creatorcontrib>Korc, Murray</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>Biochemical and biophysical research communications</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Bergmann, Uwe</au><au>Funatomi, Hitoshi</au><au>Kornmann, Marko</au><au>Beger, Hans G.</au><au>Korc, Murray</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Increased Expression of Insulin Receptor Substrate-1 in Human Pancreatic Cancer</atitle><jtitle>Biochemical and biophysical research communications</jtitle><addtitle>Biochem Biophys Res Commun</addtitle><date>1996-03-27</date><risdate>1996</risdate><volume>220</volume><issue>3</issue><spage>886</spage><epage>890</epage><pages>886-890</pages><issn>0006-291X</issn><eissn>1090-2104</eissn><abstract>Insulin receptor substrate-1 (IRS-1) is a multisite docking protein implicated in mitogenic signaling following activation of the insulin and insulin-like growth factor I receptors. In the present study we characterized IRS-1 expression in human pancreatic cancer. Northern blot analysis revealed high levels of IRS-1 mRNA transcripts in ASPC-1 and MIA PaCa-2 human pancreatic cancer cell lines, and lower levels in COLO-357, PANC-1, and T3M4 cells. Immunoblotting with anti-IRS-1 antibodies indicated that IRS-1 protein levels paralleled IRS-1 mRNA levels. Analysis of RNA isolated from normal and cancerous human pancreatic tissues indicated that 7 of 16 pancreatic cancer samples overexpressed IRS-1 mRNA transcripts by comparison with the normal pancreas and that insulin mRNA levels were abundant in many tumors. These data suggest that IRS-1 contributes to the signaling pathways that lead to excessive growth stimulation in human pancreatic cancer.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>8607861</pmid><doi>10.1006/bbrc.1996.0500</doi><tpages>5</tpages></addata></record> |
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subjects | Blotting, Northern Cell Line Colonic Neoplasms Gene Expression - drug effects Humans Insulin - biosynthesis Insulin - pharmacology Insulin Receptor Substrate Proteins Pancreas - metabolism Pancreatic Neoplasms - metabolism Phosphoproteins - biosynthesis Phosphoproteins - isolation & purification RNA, Messenger - analysis RNA, Messenger - biosynthesis Transcription, Genetic Tumor Cells, Cultured |
title | Increased Expression of Insulin Receptor Substrate-1 in Human Pancreatic Cancer |
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