The Expression of Growth Hormone-Releasing Hormone (GHRH) and Splice Variants of Its Receptor in Human Gastroenteropancreatic Carcinomas
Splice variants (SVs) of receptors for growth hormone-releasing hormone (GHRH) have been found in primary human prostate cancers and diverse human cancer cell lines. GHRH antagonists inhibit growth of various experimental human cancers, including pancreatic and colorectal, xenografted into nude mice...
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| Veröffentlicht in: | Proceedings of the National Academy of Sciences - PNAS 2002-09, Vol.99 (18), p.11866-11871 |
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| creator | Busto, Rebeca Schally, Andrew V. Varga, Jozsef L. Garcia-Fernandez, M. Olga Groot, Kate Armatis, Patricia Szepeshazi, Karoly |
| description | Splice variants (SVs) of receptors for growth hormone-releasing hormone (GHRH) have been found in primary human prostate cancers and diverse human cancer cell lines. GHRH antagonists inhibit growth of various experimental human cancers, including pancreatic and colorectal, xenografted into nude mice or cultured in vitro, and their antiproliferative action could be mediated in part through SVs of GHRH receptors. In this study we examined the expression of mRNA for GHRH and for SVs of its receptors in tumors of human pancreatic, colorectal, and gastric cancer cell lines grown in nude mice. mRNA for both GHRH and SV1isoform of GHRH receptors was expressed in tumors of pancreatic (SW1990, PANC-1, MIA PaCa-2, Capan-1, Capan-2, and CFPAC1), colonic (COLO 320DM and HT-29), and gastric (NCI-N87, HS746T, and AGS) cancer cell lines; mRNA for SV2was also present in Capan-1, Capan-2, CFPAC1, HT-29, and NCI-N87 tumors. In proliferation studies in vitro, the growth of pancreatic, colonic, and gastric cancer cells was stimulated by GHRH(1-29)NH2and inhibited by GHRH antagonist JV-1-38. The stimulation of some gastroenteropancreatic cancer cells by GHRH was followed by an increase in cAMP production, and GHRH antagonist JV-1-38 competitively inhibited this effect. Our study indicates the presence of an autocrine/paracrine stimulatory loop based on GHRH and SV1of GHRH receptors in human pancreatic, colorectal, and gastric cancers. The finding of SV1receptor in human cancers provides an approach to an antitumor therapy based on the blockade of this receptor by specific GHRH antagonists. |
| doi_str_mv | 10.1073/pnas.182433099 |
| format | Article |
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Olga ; Groot, Kate ; Armatis, Patricia ; Szepeshazi, Karoly</creator><creatorcontrib>Busto, Rebeca ; Schally, Andrew V. ; Varga, Jozsef L. ; Garcia-Fernandez, M. Olga ; Groot, Kate ; Armatis, Patricia ; Szepeshazi, Karoly</creatorcontrib><description>Splice variants (SVs) of receptors for growth hormone-releasing hormone (GHRH) have been found in primary human prostate cancers and diverse human cancer cell lines. GHRH antagonists inhibit growth of various experimental human cancers, including pancreatic and colorectal, xenografted into nude mice or cultured in vitro, and their antiproliferative action could be mediated in part through SVs of GHRH receptors. In this study we examined the expression of mRNA for GHRH and for SVs of its receptors in tumors of human pancreatic, colorectal, and gastric cancer cell lines grown in nude mice. mRNA for both GHRH and SV1isoform of GHRH receptors was expressed in tumors of pancreatic (SW1990, PANC-1, MIA PaCa-2, Capan-1, Capan-2, and CFPAC1), colonic (COLO 320DM and HT-29), and gastric (NCI-N87, HS746T, and AGS) cancer cell lines; mRNA for SV2was also present in Capan-1, Capan-2, CFPAC1, HT-29, and NCI-N87 tumors. In proliferation studies in vitro, the growth of pancreatic, colonic, and gastric cancer cells was stimulated by GHRH(1-29)NH2and inhibited by GHRH antagonist JV-1-38. The stimulation of some gastroenteropancreatic cancer cells by GHRH was followed by an increase in cAMP production, and GHRH antagonist JV-1-38 competitively inhibited this effect. Our study indicates the presence of an autocrine/paracrine stimulatory loop based on GHRH and SV1of GHRH receptors in human pancreatic, colorectal, and gastric cancers. The finding of SV1receptor in human cancers provides an approach to an antitumor therapy based on the blockade of this receptor by specific GHRH antagonists.</description><identifier>ISSN: 0027-8424</identifier><identifier>EISSN: 1091-6490</identifier><identifier>DOI: 10.1073/pnas.182433099</identifier><identifier>PMID: 12186980</identifier><language>eng</language><publisher>United States: National Academy of Sciences</publisher><subject>Animals ; Base Sequence ; Biological Sciences ; Cancer ; Cell growth ; Cell lines ; Cultured cells ; Cyclic AMP - metabolism ; Digestive system ; DNA Primers ; Gastrointestinal Neoplasms - genetics ; Gastrointestinal Neoplasms - metabolism ; Gastrointestinal Neoplasms - pathology ; Growth Hormone-Releasing Hormone - analogs & derivatives ; Growth Hormone-Releasing Hormone - antagonists & inhibitors ; Growth Hormone-Releasing Hormone - genetics ; Growth Hormone-Releasing Hormone - pharmacology ; Hormones ; Humans ; Male ; Messenger RNA ; Mice ; Mice, Nude ; Pancreatic neoplasms ; Polymerase chain reaction ; Receptors ; Receptors, Neuropeptide - genetics ; Receptors, Pituitary Hormone-Regulating Hormone - genetics ; Reverse Transcriptase Polymerase Chain Reaction ; RNA Splicing ; RNA, Messenger - genetics ; Tumor cell line ; Tumor Cells, Cultured ; Tumors</subject><ispartof>Proceedings of the National Academy of Sciences - PNAS, 2002-09, Vol.99 (18), p.11866-11871</ispartof><rights>Copyright 1993-2002 National Academy of Sciences of the United States of America</rights><rights>Copyright National Academy of Sciences Sep 3, 2002</rights><rights>Copyright © 2002, The National Academy of Sciences 2002</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c490t-b279f994fc300fe94d1dc6e10f05a56e77353245977a826102731304cb88e22f3</citedby><cites>FETCH-LOGICAL-c490t-b279f994fc300fe94d1dc6e10f05a56e77353245977a826102731304cb88e22f3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Uhttp://www.pnas.org/content/99/18.cover.gif</thumbnail><linktopdf>$$Uhttps://www.jstor.org/stable/pdf/3073130$$EPDF$$P50$$Gjstor$$H</linktopdf><linktohtml>$$Uhttps://www.jstor.org/stable/3073130$$EHTML$$P50$$Gjstor$$H</linktohtml><link.rule.ids>230,314,727,780,784,803,885,27923,27924,53790,53792,58016,58249</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12186980$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Busto, Rebeca</creatorcontrib><creatorcontrib>Schally, Andrew V.</creatorcontrib><creatorcontrib>Varga, Jozsef L.</creatorcontrib><creatorcontrib>Garcia-Fernandez, M. Olga</creatorcontrib><creatorcontrib>Groot, Kate</creatorcontrib><creatorcontrib>Armatis, Patricia</creatorcontrib><creatorcontrib>Szepeshazi, Karoly</creatorcontrib><title>The Expression of Growth Hormone-Releasing Hormone (GHRH) and Splice Variants of Its Receptor in Human Gastroenteropancreatic Carcinomas</title><title>Proceedings of the National Academy of Sciences - PNAS</title><addtitle>Proc Natl Acad Sci U S A</addtitle><description>Splice variants (SVs) of receptors for growth hormone-releasing hormone (GHRH) have been found in primary human prostate cancers and diverse human cancer cell lines. GHRH antagonists inhibit growth of various experimental human cancers, including pancreatic and colorectal, xenografted into nude mice or cultured in vitro, and their antiproliferative action could be mediated in part through SVs of GHRH receptors. In this study we examined the expression of mRNA for GHRH and for SVs of its receptors in tumors of human pancreatic, colorectal, and gastric cancer cell lines grown in nude mice. mRNA for both GHRH and SV1isoform of GHRH receptors was expressed in tumors of pancreatic (SW1990, PANC-1, MIA PaCa-2, Capan-1, Capan-2, and CFPAC1), colonic (COLO 320DM and HT-29), and gastric (NCI-N87, HS746T, and AGS) cancer cell lines; mRNA for SV2was also present in Capan-1, Capan-2, CFPAC1, HT-29, and NCI-N87 tumors. In proliferation studies in vitro, the growth of pancreatic, colonic, and gastric cancer cells was stimulated by GHRH(1-29)NH2and inhibited by GHRH antagonist JV-1-38. The stimulation of some gastroenteropancreatic cancer cells by GHRH was followed by an increase in cAMP production, and GHRH antagonist JV-1-38 competitively inhibited this effect. Our study indicates the presence of an autocrine/paracrine stimulatory loop based on GHRH and SV1of GHRH receptors in human pancreatic, colorectal, and gastric cancers. The finding of SV1receptor in human cancers provides an approach to an antitumor therapy based on the blockade of this receptor by specific GHRH antagonists.</description><subject>Animals</subject><subject>Base Sequence</subject><subject>Biological Sciences</subject><subject>Cancer</subject><subject>Cell growth</subject><subject>Cell lines</subject><subject>Cultured cells</subject><subject>Cyclic AMP - metabolism</subject><subject>Digestive system</subject><subject>DNA Primers</subject><subject>Gastrointestinal Neoplasms - genetics</subject><subject>Gastrointestinal Neoplasms - metabolism</subject><subject>Gastrointestinal Neoplasms - pathology</subject><subject>Growth Hormone-Releasing Hormone - analogs & derivatives</subject><subject>Growth Hormone-Releasing Hormone - antagonists & inhibitors</subject><subject>Growth Hormone-Releasing Hormone - genetics</subject><subject>Growth Hormone-Releasing Hormone - pharmacology</subject><subject>Hormones</subject><subject>Humans</subject><subject>Male</subject><subject>Messenger RNA</subject><subject>Mice</subject><subject>Mice, Nude</subject><subject>Pancreatic neoplasms</subject><subject>Polymerase chain reaction</subject><subject>Receptors</subject><subject>Receptors, Neuropeptide - genetics</subject><subject>Receptors, Pituitary Hormone-Regulating Hormone - genetics</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><subject>RNA Splicing</subject><subject>RNA, Messenger - genetics</subject><subject>Tumor cell line</subject><subject>Tumor Cells, Cultured</subject><subject>Tumors</subject><issn>0027-8424</issn><issn>1091-6490</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2002</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kU1vEzEQhlcIREPhygmB1QMqhw1je7984FBFJalUCSkUrpbjzDaOdu3F9kL5B_xsHJKGjwOnkWaed_TOvFn2nMKUQs3fDlaFKW1YwTkI8SCbUBA0rwoBD7MJAKvzpmDFSfYkhC0AiLKBx9kJZbSpRAOT7MfNBsnl3eAxBOMscS2Ze_ctbsjC-d5ZzJfYoQrG3t53yPl8sVy8IcquycehMxrJZ-WNsjHs5FepLFHjEJ0nxpLF2CtL5ipE79BG9G5QVntU0WgyU14b63oVnmaPWtUFfHaop9mn95c3s0V-_WF-Nbu4znW6KeYrVotWiKLVHKBFUazpWldIoYVSlRXWNS85K0pR16phFU0f4JRDoVdNg4y1_DR7t987jKse1zpZ8qqTgze98t-lU0b-PbFmI2_dV0mZ4BUk_euD3rsvI4YoexM0dp2y6MYgawZlycomgWf_gFs3eptukwxoweualQma7iHtXQge26MRCnIXsNwFLI8BJ8HLP-3_xg-JJuDVAdgJ78dCpB2SJqZKxPn_CdmOXRfxLib0xR7dhpTmkeXw66n8J_RKxCY</recordid><startdate>20020903</startdate><enddate>20020903</enddate><creator>Busto, Rebeca</creator><creator>Schally, Andrew V.</creator><creator>Varga, Jozsef L.</creator><creator>Garcia-Fernandez, M. 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Olga</au><au>Groot, Kate</au><au>Armatis, Patricia</au><au>Szepeshazi, Karoly</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The Expression of Growth Hormone-Releasing Hormone (GHRH) and Splice Variants of Its Receptor in Human Gastroenteropancreatic Carcinomas</atitle><jtitle>Proceedings of the National Academy of Sciences - PNAS</jtitle><addtitle>Proc Natl Acad Sci U S A</addtitle><date>2002-09-03</date><risdate>2002</risdate><volume>99</volume><issue>18</issue><spage>11866</spage><epage>11871</epage><pages>11866-11871</pages><issn>0027-8424</issn><eissn>1091-6490</eissn><abstract>Splice variants (SVs) of receptors for growth hormone-releasing hormone (GHRH) have been found in primary human prostate cancers and diverse human cancer cell lines. GHRH antagonists inhibit growth of various experimental human cancers, including pancreatic and colorectal, xenografted into nude mice or cultured in vitro, and their antiproliferative action could be mediated in part through SVs of GHRH receptors. In this study we examined the expression of mRNA for GHRH and for SVs of its receptors in tumors of human pancreatic, colorectal, and gastric cancer cell lines grown in nude mice. mRNA for both GHRH and SV1isoform of GHRH receptors was expressed in tumors of pancreatic (SW1990, PANC-1, MIA PaCa-2, Capan-1, Capan-2, and CFPAC1), colonic (COLO 320DM and HT-29), and gastric (NCI-N87, HS746T, and AGS) cancer cell lines; mRNA for SV2was also present in Capan-1, Capan-2, CFPAC1, HT-29, and NCI-N87 tumors. In proliferation studies in vitro, the growth of pancreatic, colonic, and gastric cancer cells was stimulated by GHRH(1-29)NH2and inhibited by GHRH antagonist JV-1-38. The stimulation of some gastroenteropancreatic cancer cells by GHRH was followed by an increase in cAMP production, and GHRH antagonist JV-1-38 competitively inhibited this effect. Our study indicates the presence of an autocrine/paracrine stimulatory loop based on GHRH and SV1of GHRH receptors in human pancreatic, colorectal, and gastric cancers. The finding of SV1receptor in human cancers provides an approach to an antitumor therapy based on the blockade of this receptor by specific GHRH antagonists.</abstract><cop>United States</cop><pub>National Academy of Sciences</pub><pmid>12186980</pmid><doi>10.1073/pnas.182433099</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Base Sequence Biological Sciences Cancer Cell growth Cell lines Cultured cells Cyclic AMP - metabolism Digestive system DNA Primers Gastrointestinal Neoplasms - genetics Gastrointestinal Neoplasms - metabolism Gastrointestinal Neoplasms - pathology Growth Hormone-Releasing Hormone - analogs & derivatives Growth Hormone-Releasing Hormone - antagonists & inhibitors Growth Hormone-Releasing Hormone - genetics Growth Hormone-Releasing Hormone - pharmacology Hormones Humans Male Messenger RNA Mice Mice, Nude Pancreatic neoplasms Polymerase chain reaction Receptors Receptors, Neuropeptide - genetics Receptors, Pituitary Hormone-Regulating Hormone - genetics Reverse Transcriptase Polymerase Chain Reaction RNA Splicing RNA, Messenger - genetics Tumor cell line Tumor Cells, Cultured Tumors |
| title | The Expression of Growth Hormone-Releasing Hormone (GHRH) and Splice Variants of Its Receptor in Human Gastroenteropancreatic Carcinomas |
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