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Meningiomas expressing and responding to cholecystokinin (CCK)
The effect of cholecystokinin (CCK) on cultured human meningioma derived cells was investigated. Exposure of meningioma cells for 6-12 days to CCK-8s (2-200 nM) resulted in a dose dependent stimulation of cell growth to a maximum of 1.1-fold over basal controls. A time course study showed stimulatio...
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Published in: | Journal of neuro-oncology 2005-07, Vol.73 (3), p.199-204 |
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creator | OIKONOMOU, Eftychia MACHADO, Ana L BUCHFELDER, Michael ADAMS, Eric F |
description | The effect of cholecystokinin (CCK) on cultured human meningioma derived cells was investigated. Exposure of meningioma cells for 6-12 days to CCK-8s (2-200 nM) resulted in a dose dependent stimulation of cell growth to a maximum of 1.1-fold over basal controls. A time course study showed stimulation of cell growth at day 3 followed by increase throughout day 6. The stimulatory effect of CCK on meningioma cell growth was completely abolished by a CCK-B specific receptor antagonist, L-365,260. Reverse-transcription of meningioma-derived RNA into cDNA followed by amplification by the polymerase chain reaction using specific primers for CCK peptide and its CCK-A and/B receptor revealed 100% presence of CCK peptide and CCK-B receptors mRNA whereas CCK-A receptor was expressed in 66% of the meningiomas. These results provide evidence that human meningioma cells possess CCK peptide and its receptors the activation of which leads to increase of cell growth possibly via an autocrine/paracrine mechanism. |
doi_str_mv | 10.1007/s11060-004-5177-2 |
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Exposure of meningioma cells for 6-12 days to CCK-8s (2-200 nM) resulted in a dose dependent stimulation of cell growth to a maximum of 1.1-fold over basal controls. A time course study showed stimulation of cell growth at day 3 followed by increase throughout day 6. The stimulatory effect of CCK on meningioma cell growth was completely abolished by a CCK-B specific receptor antagonist, L-365,260. Reverse-transcription of meningioma-derived RNA into cDNA followed by amplification by the polymerase chain reaction using specific primers for CCK peptide and its CCK-A and/B receptor revealed 100% presence of CCK peptide and CCK-B receptors mRNA whereas CCK-A receptor was expressed in 66% of the meningiomas. These results provide evidence that human meningioma cells possess CCK peptide and its receptors the activation of which leads to increase of cell growth possibly via an autocrine/paracrine mechanism.</description><identifier>ISSN: 0167-594X</identifier><identifier>EISSN: 1573-7373</identifier><identifier>DOI: 10.1007/s11060-004-5177-2</identifier><identifier>PMID: 15980969</identifier><identifier>CODEN: JNODD2</identifier><language>eng</language><publisher>Dordrecht: Springer</publisher><subject>Adult ; Base Sequence ; Benzodiazepinones - pharmacology ; Biological and medical sciences ; Cell Proliferation - drug effects ; Cells, Cultured ; Cholecystokinin - genetics ; Cholecystokinin - metabolism ; Cholecystokinin - pharmacology ; Female ; Humans ; Male ; Medical sciences ; Meningeal Neoplasms - genetics ; Meningeal Neoplasms - metabolism ; Meningioma - genetics ; Meningioma - metabolism ; Middle Aged ; Molecular Sequence Data ; Neurology ; Neurosurgery ; Phenylurea Compounds - pharmacology ; Receptors, Cholecystokinin - antagonists & inhibitors ; Receptors, Cholecystokinin - metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; RNA, Messenger - analysis ; Skull, brain, vascular surgery ; Surgery (general aspects). Transplantations, organ and tissue grafts. Graft diseases ; Time Factors ; Tumors of the nervous system. Phacomatoses</subject><ispartof>Journal of neuro-oncology, 2005-07, Vol.73 (3), p.199-204</ispartof><rights>2005 INIST-CNRS</rights><rights>Springer 2005</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c387t-f125b9d3c158dfbe3e6a2c8bdf3390789b5fd6d2cd5300c86b5ddb69f3b8ea4d3</citedby><cites>FETCH-LOGICAL-c387t-f125b9d3c158dfbe3e6a2c8bdf3390789b5fd6d2cd5300c86b5ddb69f3b8ea4d3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=16963335$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15980969$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>OIKONOMOU, Eftychia</creatorcontrib><creatorcontrib>MACHADO, Ana L</creatorcontrib><creatorcontrib>BUCHFELDER, Michael</creatorcontrib><creatorcontrib>ADAMS, Eric F</creatorcontrib><title>Meningiomas expressing and responding to cholecystokinin (CCK)</title><title>Journal of neuro-oncology</title><addtitle>J Neurooncol</addtitle><description>The effect of cholecystokinin (CCK) on cultured human meningioma derived cells was investigated. Exposure of meningioma cells for 6-12 days to CCK-8s (2-200 nM) resulted in a dose dependent stimulation of cell growth to a maximum of 1.1-fold over basal controls. A time course study showed stimulation of cell growth at day 3 followed by increase throughout day 6. The stimulatory effect of CCK on meningioma cell growth was completely abolished by a CCK-B specific receptor antagonist, L-365,260. Reverse-transcription of meningioma-derived RNA into cDNA followed by amplification by the polymerase chain reaction using specific primers for CCK peptide and its CCK-A and/B receptor revealed 100% presence of CCK peptide and CCK-B receptors mRNA whereas CCK-A receptor was expressed in 66% of the meningiomas. These results provide evidence that human meningioma cells possess CCK peptide and its receptors the activation of which leads to increase of cell growth possibly via an autocrine/paracrine mechanism.</description><subject>Adult</subject><subject>Base Sequence</subject><subject>Benzodiazepinones - pharmacology</subject><subject>Biological and medical sciences</subject><subject>Cell Proliferation - drug effects</subject><subject>Cells, Cultured</subject><subject>Cholecystokinin - genetics</subject><subject>Cholecystokinin - metabolism</subject><subject>Cholecystokinin - pharmacology</subject><subject>Female</subject><subject>Humans</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Meningeal Neoplasms - genetics</subject><subject>Meningeal Neoplasms - metabolism</subject><subject>Meningioma - genetics</subject><subject>Meningioma - metabolism</subject><subject>Middle Aged</subject><subject>Molecular Sequence Data</subject><subject>Neurology</subject><subject>Neurosurgery</subject><subject>Phenylurea Compounds - pharmacology</subject><subject>Receptors, Cholecystokinin - antagonists & inhibitors</subject><subject>Receptors, Cholecystokinin - metabolism</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><subject>RNA, Messenger - analysis</subject><subject>Skull, brain, vascular surgery</subject><subject>Surgery (general aspects). Transplantations, organ and tissue grafts. Graft diseases</subject><subject>Time Factors</subject><subject>Tumors of the nervous system. Phacomatoses</subject><issn>0167-594X</issn><issn>1573-7373</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><recordid>eNqFkUtLxDAUhYMozvj4AW6kCIouqklv89oIMvjCETcK7kKapNqx09SmBeffm2EGBty4uvfCdw7ccxA6IviSYMyvAiGY4RTjPKWE8zTbQmNCOaQcOGyjMSaMp1Tm7yO0F8IMR5AD2UUjQqXAkskxun52TdV8VH6uQ-J-2s6FEO9ENzaJe-sbuzx7n5hPXzuzCL3_qqIkOZ9Mni4O0E6p6-AO13Mfvd3dvk4e0unL_ePkZpoaELxPS5LRQlowhApbFg4c05kRhS0BJOZCFrS0zGbGUsDYCFZQawsmSyiE07mFfXS28m07_z240Kt5FYyra904PwTFuOQ5SPgXJBxLyQWO4MkfcOaHrolPqIxICnlGlxBZQabzIXSuVG1XzXW3UASrZQVqVYGKyaplBSqLmuO18VDMnd0o1plH4HQN6GB0XXa6MVXYcEwyAKDwC_wVjfc</recordid><startdate>20050701</startdate><enddate>20050701</enddate><creator>OIKONOMOU, Eftychia</creator><creator>MACHADO, Ana L</creator><creator>BUCHFELDER, Michael</creator><creator>ADAMS, Eric F</creator><general>Springer</general><general>Springer Nature B.V</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>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope></search><sort><creationdate>20050701</creationdate><title>Meningiomas expressing and responding to cholecystokinin (CCK)</title><author>OIKONOMOU, Eftychia ; MACHADO, Ana L ; BUCHFELDER, Michael ; ADAMS, Eric F</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c387t-f125b9d3c158dfbe3e6a2c8bdf3390789b5fd6d2cd5300c86b5ddb69f3b8ea4d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Adult</topic><topic>Base Sequence</topic><topic>Benzodiazepinones - pharmacology</topic><topic>Biological and medical sciences</topic><topic>Cell Proliferation - drug effects</topic><topic>Cells, Cultured</topic><topic>Cholecystokinin - genetics</topic><topic>Cholecystokinin - metabolism</topic><topic>Cholecystokinin - pharmacology</topic><topic>Female</topic><topic>Humans</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Meningeal Neoplasms - genetics</topic><topic>Meningeal Neoplasms - metabolism</topic><topic>Meningioma - genetics</topic><topic>Meningioma - metabolism</topic><topic>Middle Aged</topic><topic>Molecular Sequence Data</topic><topic>Neurology</topic><topic>Neurosurgery</topic><topic>Phenylurea Compounds - pharmacology</topic><topic>Receptors, Cholecystokinin - antagonists & inhibitors</topic><topic>Receptors, Cholecystokinin - metabolism</topic><topic>Reverse Transcriptase Polymerase Chain Reaction</topic><topic>RNA, Messenger - analysis</topic><topic>Skull, brain, vascular surgery</topic><topic>Surgery (general aspects). Transplantations, organ and tissue grafts. Graft diseases</topic><topic>Time Factors</topic><topic>Tumors of the nervous system. Phacomatoses</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>OIKONOMOU, Eftychia</creatorcontrib><creatorcontrib>MACHADO, Ana L</creatorcontrib><creatorcontrib>BUCHFELDER, Michael</creatorcontrib><creatorcontrib>ADAMS, Eric F</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>Neurosciences Abstracts</collection><collection>ProQuest Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central</collection><collection>AUTh Library subscriptions: ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</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>MEDLINE - Academic</collection><jtitle>Journal of neuro-oncology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>OIKONOMOU, Eftychia</au><au>MACHADO, Ana L</au><au>BUCHFELDER, Michael</au><au>ADAMS, Eric F</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Meningiomas expressing and responding to cholecystokinin (CCK)</atitle><jtitle>Journal of neuro-oncology</jtitle><addtitle>J Neurooncol</addtitle><date>2005-07-01</date><risdate>2005</risdate><volume>73</volume><issue>3</issue><spage>199</spage><epage>204</epage><pages>199-204</pages><issn>0167-594X</issn><eissn>1573-7373</eissn><coden>JNODD2</coden><abstract>The effect of cholecystokinin (CCK) on cultured human meningioma derived cells was investigated. Exposure of meningioma cells for 6-12 days to CCK-8s (2-200 nM) resulted in a dose dependent stimulation of cell growth to a maximum of 1.1-fold over basal controls. A time course study showed stimulation of cell growth at day 3 followed by increase throughout day 6. The stimulatory effect of CCK on meningioma cell growth was completely abolished by a CCK-B specific receptor antagonist, L-365,260. Reverse-transcription of meningioma-derived RNA into cDNA followed by amplification by the polymerase chain reaction using specific primers for CCK peptide and its CCK-A and/B receptor revealed 100% presence of CCK peptide and CCK-B receptors mRNA whereas CCK-A receptor was expressed in 66% of the meningiomas. These results provide evidence that human meningioma cells possess CCK peptide and its receptors the activation of which leads to increase of cell growth possibly via an autocrine/paracrine mechanism.</abstract><cop>Dordrecht</cop><pub>Springer</pub><pmid>15980969</pmid><doi>10.1007/s11060-004-5177-2</doi><tpages>6</tpages></addata></record> |
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subjects | Adult Base Sequence Benzodiazepinones - pharmacology Biological and medical sciences Cell Proliferation - drug effects Cells, Cultured Cholecystokinin - genetics Cholecystokinin - metabolism Cholecystokinin - pharmacology Female Humans Male Medical sciences Meningeal Neoplasms - genetics Meningeal Neoplasms - metabolism Meningioma - genetics Meningioma - metabolism Middle Aged Molecular Sequence Data Neurology Neurosurgery Phenylurea Compounds - pharmacology Receptors, Cholecystokinin - antagonists & inhibitors Receptors, Cholecystokinin - metabolism Reverse Transcriptase Polymerase Chain Reaction RNA, Messenger - analysis Skull, brain, vascular surgery Surgery (general aspects). Transplantations, organ and tissue grafts. Graft diseases Time Factors Tumors of the nervous system. Phacomatoses |
title | Meningiomas expressing and responding to cholecystokinin (CCK) |
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