Uptake of the carborane derivative of cholesteryl ester by glioma cancer cells is mediated through LDL receptors
This study was to elucidate the mechanism of cellular uptake of cholesteryl 1,12-dicarba-closo-dodecaboranel-carboxylate (BCH), a new anti-cancer carborane derivative of cholesteryl ester, by glioma cancer cells. BCH (solubilized with liposomal formulation) was incubated with SF-763 and SF-767 gliom...
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Veröffentlicht in: | Pharmaceutical research 2004-07, Vol.21 (7), p.1257-1262 |
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creator | Pan, Guangliang Oie, Svein Lu, D Robert |
description | This study was to elucidate the mechanism of cellular uptake of cholesteryl 1,12-dicarba-closo-dodecaboranel-carboxylate (BCH), a new anti-cancer carborane derivative of cholesteryl ester, by glioma cancer cells.
BCH (solubilized with liposomal formulation) was incubated with SF-763 and SF-767 glioma cell lines in the presence of different amounts of monoclonal anti-LDL receptor antibody for cellular uptake studies. Various amounts of lipoprotein deficient serum (LPDS) were also used during the uptake. The effect of calcium ion and low temperature on BCH uptake were investigated. In addition, the transfer of BCH from liposomes to low-density lipoprotein (LDL) particles was determined through gradient ultracentrifugation.
BCH uptake by these glioma cells was significantly inhibited by the monoclonal antibody. The uptake by both cell lines was reversely correlated with the amount of LPDS. The presence of calcium ion promoted the BCH uptake, whereas the low temperature decreased the BCH uptake. After 16 h incubation, about 46% of BCH was transferred from liposomes to LDL particles.
These results strongly suggested that the cellular uptake of BCH (in liposomal formulation) by SF-763 and SF-767 glioma cell lines is mediated through LDL receptors. |
doi_str_mv | 10.1023/b:pham.0000033014.04820.a7 |
format | Article |
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BCH (solubilized with liposomal formulation) was incubated with SF-763 and SF-767 glioma cell lines in the presence of different amounts of monoclonal anti-LDL receptor antibody for cellular uptake studies. Various amounts of lipoprotein deficient serum (LPDS) were also used during the uptake. The effect of calcium ion and low temperature on BCH uptake were investigated. In addition, the transfer of BCH from liposomes to low-density lipoprotein (LDL) particles was determined through gradient ultracentrifugation.
BCH uptake by these glioma cells was significantly inhibited by the monoclonal antibody. The uptake by both cell lines was reversely correlated with the amount of LPDS. The presence of calcium ion promoted the BCH uptake, whereas the low temperature decreased the BCH uptake. After 16 h incubation, about 46% of BCH was transferred from liposomes to LDL particles.
These results strongly suggested that the cellular uptake of BCH (in liposomal formulation) by SF-763 and SF-767 glioma cell lines is mediated through LDL receptors.</description><identifier>ISSN: 0724-8741</identifier><identifier>EISSN: 1573-904X</identifier><identifier>DOI: 10.1023/b:pham.0000033014.04820.a7</identifier><identifier>PMID: 15290868</identifier><language>eng</language><publisher>United States: Springer Nature B.V</publisher><subject>Antibodies ; Antibodies, Monoclonal - isolation & purification ; Antibodies, Monoclonal - pharmacology ; Boron Compounds - administration & dosage ; Boron Compounds - pharmacokinetics ; Brain cancer ; Calcium - metabolism ; Cancer therapies ; Cell culture ; Cell growth ; Cell Line, Tumor ; Cholesterol ; Cholesterol Esters - administration & dosage ; Cholesterol Esters - pharmacokinetics ; Chromatography, High Pressure Liquid ; Cold Temperature ; Dose-Response Relationship, Drug ; Electrophoresis, Polyacrylamide Gel ; Glioma ; Humans ; Laboratories ; Ligands ; Lipoproteins ; Lipoproteins, LDL - metabolism ; Liposomes ; Low density lipoprotein receptors ; Receptors, LDL - antagonists & inhibitors ; Receptors, LDL - physiology</subject><ispartof>Pharmaceutical research, 2004-07, Vol.21 (7), p.1257-1262</ispartof><rights>Copyright Kluwer Academic Publishers Jul 2004</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c408t-b54ea14b26ae1d89c3969ce4c23801556211bffc3a81c1136e4936635335bbd33</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15290868$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Pan, Guangliang</creatorcontrib><creatorcontrib>Oie, Svein</creatorcontrib><creatorcontrib>Lu, D Robert</creatorcontrib><title>Uptake of the carborane derivative of cholesteryl ester by glioma cancer cells is mediated through LDL receptors</title><title>Pharmaceutical research</title><addtitle>Pharm Res</addtitle><description>This study was to elucidate the mechanism of cellular uptake of cholesteryl 1,12-dicarba-closo-dodecaboranel-carboxylate (BCH), a new anti-cancer carborane derivative of cholesteryl ester, by glioma cancer cells.
BCH (solubilized with liposomal formulation) was incubated with SF-763 and SF-767 glioma cell lines in the presence of different amounts of monoclonal anti-LDL receptor antibody for cellular uptake studies. Various amounts of lipoprotein deficient serum (LPDS) were also used during the uptake. The effect of calcium ion and low temperature on BCH uptake were investigated. In addition, the transfer of BCH from liposomes to low-density lipoprotein (LDL) particles was determined through gradient ultracentrifugation.
BCH uptake by these glioma cells was significantly inhibited by the monoclonal antibody. The uptake by both cell lines was reversely correlated with the amount of LPDS. The presence of calcium ion promoted the BCH uptake, whereas the low temperature decreased the BCH uptake. After 16 h incubation, about 46% of BCH was transferred from liposomes to LDL particles.
These results strongly suggested that the cellular uptake of BCH (in liposomal formulation) by SF-763 and SF-767 glioma cell lines is mediated through LDL receptors.</description><subject>Antibodies</subject><subject>Antibodies, Monoclonal - isolation & purification</subject><subject>Antibodies, Monoclonal - pharmacology</subject><subject>Boron Compounds - administration & dosage</subject><subject>Boron Compounds - pharmacokinetics</subject><subject>Brain cancer</subject><subject>Calcium - metabolism</subject><subject>Cancer therapies</subject><subject>Cell culture</subject><subject>Cell growth</subject><subject>Cell Line, Tumor</subject><subject>Cholesterol</subject><subject>Cholesterol Esters - administration & dosage</subject><subject>Cholesterol Esters - pharmacokinetics</subject><subject>Chromatography, High Pressure Liquid</subject><subject>Cold Temperature</subject><subject>Dose-Response Relationship, Drug</subject><subject>Electrophoresis, Polyacrylamide Gel</subject><subject>Glioma</subject><subject>Humans</subject><subject>Laboratories</subject><subject>Ligands</subject><subject>Lipoproteins</subject><subject>Lipoproteins, LDL - metabolism</subject><subject>Liposomes</subject><subject>Low density lipoprotein receptors</subject><subject>Receptors, LDL - antagonists & inhibitors</subject><subject>Receptors, LDL - physiology</subject><issn>0724-8741</issn><issn>1573-904X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNpdkU1LxDAQhoMoun78BQkevHXNV9PUm98KK3pQ8BaSdOpW201NWmH_vdl1QTCXgcwzM-_Mi9AJJVNKGD-z5_3cdFOyepwTKqZEKEampthCE5oXPCuJeNtGE1IwkalC0D20H-NHwhUtxS7aozkriZJqgvrXfjCfgH2NhzlgZ4L1wSwAVxCabzM03-ucm_sW4gBh2eJ1xHaJ39vGdybVLFz6cNC2ETcRd1A1ZoAqNQx-fJ_j2fUMB3DQDz7EQ7RTmzbC0SYeoNfbm5er-2z2dPdwdTHLnCBqyGwuwFBhmTRAK1U6XsrSgXCMK0LzXDJKbV07bhR1lHIJouRS8pzz3NqK8wN0-tu3D_5rTJp118SVxrScH6OWspBFLooEnvwDP_wYFkmbZoxJyUhRJuj8F3LBxxig1n1oOhOWmhK9MkVf6uf7i0f9Z4pem6LNasLxZsJo03H-Sjcu8B9lp4mv</recordid><startdate>200407</startdate><enddate>200407</enddate><creator>Pan, Guangliang</creator><creator>Oie, Svein</creator><creator>Lu, D Robert</creator><general>Springer Nature B.V</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>3V.</scope><scope>7RV</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</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>KB0</scope><scope>M0S</scope><scope>M1P</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope></search><sort><creationdate>200407</creationdate><title>Uptake of the carborane derivative of cholesteryl ester by glioma cancer cells is mediated through LDL receptors</title><author>Pan, Guangliang ; Oie, Svein ; Lu, D Robert</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c408t-b54ea14b26ae1d89c3969ce4c23801556211bffc3a81c1136e4936635335bbd33</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>Antibodies</topic><topic>Antibodies, Monoclonal - isolation & purification</topic><topic>Antibodies, Monoclonal - pharmacology</topic><topic>Boron Compounds - administration & dosage</topic><topic>Boron Compounds - pharmacokinetics</topic><topic>Brain cancer</topic><topic>Calcium - metabolism</topic><topic>Cancer therapies</topic><topic>Cell culture</topic><topic>Cell growth</topic><topic>Cell Line, Tumor</topic><topic>Cholesterol</topic><topic>Cholesterol Esters - administration & dosage</topic><topic>Cholesterol Esters - pharmacokinetics</topic><topic>Chromatography, High Pressure Liquid</topic><topic>Cold Temperature</topic><topic>Dose-Response Relationship, Drug</topic><topic>Electrophoresis, Polyacrylamide Gel</topic><topic>Glioma</topic><topic>Humans</topic><topic>Laboratories</topic><topic>Ligands</topic><topic>Lipoproteins</topic><topic>Lipoproteins, LDL - metabolism</topic><topic>Liposomes</topic><topic>Low density lipoprotein receptors</topic><topic>Receptors, LDL - antagonists & inhibitors</topic><topic>Receptors, LDL - physiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Pan, Guangliang</creatorcontrib><creatorcontrib>Oie, Svein</creatorcontrib><creatorcontrib>Lu, D Robert</creatorcontrib><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>Nursing & Allied Health Database</collection><collection>Neurosciences Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</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 Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>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>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Nursing & Allied Health Premium</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>Pharmaceutical research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Pan, Guangliang</au><au>Oie, Svein</au><au>Lu, D Robert</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Uptake of the carborane derivative of cholesteryl ester by glioma cancer cells is mediated through LDL receptors</atitle><jtitle>Pharmaceutical research</jtitle><addtitle>Pharm Res</addtitle><date>2004-07</date><risdate>2004</risdate><volume>21</volume><issue>7</issue><spage>1257</spage><epage>1262</epage><pages>1257-1262</pages><issn>0724-8741</issn><eissn>1573-904X</eissn><abstract>This study was to elucidate the mechanism of cellular uptake of cholesteryl 1,12-dicarba-closo-dodecaboranel-carboxylate (BCH), a new anti-cancer carborane derivative of cholesteryl ester, by glioma cancer cells.
BCH (solubilized with liposomal formulation) was incubated with SF-763 and SF-767 glioma cell lines in the presence of different amounts of monoclonal anti-LDL receptor antibody for cellular uptake studies. Various amounts of lipoprotein deficient serum (LPDS) were also used during the uptake. The effect of calcium ion and low temperature on BCH uptake were investigated. In addition, the transfer of BCH from liposomes to low-density lipoprotein (LDL) particles was determined through gradient ultracentrifugation.
BCH uptake by these glioma cells was significantly inhibited by the monoclonal antibody. The uptake by both cell lines was reversely correlated with the amount of LPDS. The presence of calcium ion promoted the BCH uptake, whereas the low temperature decreased the BCH uptake. After 16 h incubation, about 46% of BCH was transferred from liposomes to LDL particles.
These results strongly suggested that the cellular uptake of BCH (in liposomal formulation) by SF-763 and SF-767 glioma cell lines is mediated through LDL receptors.</abstract><cop>United States</cop><pub>Springer Nature B.V</pub><pmid>15290868</pmid><doi>10.1023/b:pham.0000033014.04820.a7</doi><tpages>6</tpages></addata></record> |
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subjects | Antibodies Antibodies, Monoclonal - isolation & purification Antibodies, Monoclonal - pharmacology Boron Compounds - administration & dosage Boron Compounds - pharmacokinetics Brain cancer Calcium - metabolism Cancer therapies Cell culture Cell growth Cell Line, Tumor Cholesterol Cholesterol Esters - administration & dosage Cholesterol Esters - pharmacokinetics Chromatography, High Pressure Liquid Cold Temperature Dose-Response Relationship, Drug Electrophoresis, Polyacrylamide Gel Glioma Humans Laboratories Ligands Lipoproteins Lipoproteins, LDL - metabolism Liposomes Low density lipoprotein receptors Receptors, LDL - antagonists & inhibitors Receptors, LDL - physiology |
title | Uptake of the carborane derivative of cholesteryl ester by glioma cancer cells is mediated through LDL receptors |
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