Lipofectin enhances cellular uptake of antisense DNA while inhibiting tumor cell growth.
Identifieur interne : 000225 ( Ncbi/Merge ); précédent : 000224; suivant : 000226Lipofectin enhances cellular uptake of antisense DNA while inhibiting tumor cell growth.
Auteurs : L C Yeoman [États-Unis] ; Y J Danels ; M J LynchSource :
- Antisense research and development [ 1050-5261 ] ; 1992.
Descripteurs français
- KwdFr :
- ADN antisens (métabolisme), Cellules cancéreuses en culture, Chloramphenicol O-acetyltransferase (génétique), Chloramphenicol O-acetyltransferase (métabolisme), Cinétique, Division cellulaire (), Données de séquences moléculaires, Facteur de croissance transformant alpha (biosynthèse), Facteur de croissance transformant alpha (génétique), Facteur de croissance épidermique (pharmacologie), Humains, Insuline (pharmacologie), Lignée cellulaire, Oligonucléotides antisens (métabolisme), Oligonucléotides antisens (synthèse chimique), Phosphatidyléthanolamine (pharmacologie), Régions promotrices (génétique) (), Séquence nucléotidique, Transfection, Transport biologique (), Tumeurs du côlon.
- MESH :
- biosynthèse : Facteur de croissance transformant alpha.
- génétique : Chloramphenicol O-acetyltransferase, Facteur de croissance transformant alpha.
- métabolisme : ADN antisens, Chloramphenicol O-acetyltransferase, Oligonucléotides antisens.
- pharmacologie : Facteur de croissance épidermique, Insuline, Phosphatidyléthanolamine.
- synthèse chimique : Oligonucléotides antisens.
- Cellules cancéreuses en culture, Cinétique, Division cellulaire, Données de séquences moléculaires, Humains, Lignée cellulaire, Régions promotrices (génétique), Séquence nucléotidique, Transfection, Transport biologique, Tumeurs du côlon.
English descriptors
- KwdEn :
- Base Sequence, Biological Transport (drug effects), Cell Division (drug effects), Cell Line, Chloramphenicol O-Acetyltransferase (genetics), Chloramphenicol O-Acetyltransferase (metabolism), Colonic Neoplasms, DNA, Antisense (metabolism), Epidermal Growth Factor (pharmacology), Humans, Insulin (pharmacology), Kinetics, Molecular Sequence Data, Oligonucleotides, Antisense (chemical synthesis), Oligonucleotides, Antisense (metabolism), Phosphatidylethanolamines (pharmacology), Promoter Regions, Genetic (drug effects), Transfection, Transforming Growth Factor alpha (biosynthesis), Transforming Growth Factor alpha (genetics), Tumor Cells, Cultured.
- MESH :
- chemical , biosynthesis : Transforming Growth Factor alpha.
- chemical , chemical synthesis : Oligonucleotides, Antisense.
- chemical , genetics : Chloramphenicol O-Acetyltransferase, Transforming Growth Factor alpha.
- drug effects : Biological Transport, Cell Division, Promoter Regions, Genetic.
- chemical , metabolism : Chloramphenicol O-Acetyltransferase, DNA, Antisense, Oligonucleotides, Antisense.
- chemical , pharmacology : Epidermal Growth Factor, Insulin, Phosphatidylethanolamines.
- Base Sequence, Cell Line, Colonic Neoplasms, Humans, Kinetics, Molecular Sequence Data, Transfection, Tumor Cells, Cultured.
Abstract
A natural DNA oligomer (15-mer) was synthesized with a sequence complementary to the translation initiation codon region of the human TGF-alpha mRNA and mixed with Lipofectin to form unilamellar complexes. It was found that tumor cell growth was inhibited when HCT116 cells were treated with Lipofectin-DNA oligomer complexes or with Lipofectin alone. Uptake of 32P-labeled 15-mers into colon tumor cells was compared in the presence and absence of Lipofectin. The amount of labeled oligomer found in cells that received optimal ratios of Lipofectin to DNA was 4- to 10-fold higher than the amount found in cells that received 32P-labeled DNA alone. Although Lipofectin-antisense DNA oligomer treatment of HCT116 cells caused a dose-dependent inhibition of cell growth, there was a subsequent rise in target mRNA product. Because the mechanism of growth inhibition could not involve an inhibition of TGF-alpha expression, it was concluded that Lipofectin probably exerts a nonspecific, detergent-like effect upon the cell membrane, producing an enhancement of TGF-alpha processing and release.
DOI: 10.1089/ard.1992.2.51
PubMed: 1422086
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pubmed:1422086Le document en format XML
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O-Acetyltransferase (metabolism)</term><term>Colonic Neoplasms</term><term>DNA, Antisense (metabolism)</term><term>Epidermal Growth Factor (pharmacology)</term><term>Humans</term><term>Insulin (pharmacology)</term><term>Kinetics</term><term>Molecular Sequence Data</term><term>Oligonucleotides, Antisense (chemical synthesis)</term><term>Oligonucleotides, Antisense (metabolism)</term><term>Phosphatidylethanolamines (pharmacology)</term><term>Promoter Regions, Genetic (drug effects)</term><term>Transfection</term><term>Transforming Growth Factor alpha (biosynthesis)</term><term>Transforming Growth Factor alpha (genetics)</term><term>Tumor Cells, Cultured</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>ADN antisens (métabolisme)</term><term>Cellules cancéreuses en culture</term><term>Chloramphenicol O-acetyltransferase (génétique)</term><term>Chloramphenicol O-acetyltransferase (métabolisme)</term><term>Cinétique</term><term>Division cellulaire ()</term><term>Données de séquences moléculaires</term><term>Facteur de croissance transformant alpha (biosynthèse)</term><term>Facteur de croissance transformant alpha (génétique)</term><term>Facteur de croissance épidermique (pharmacologie)</term><term>Humains</term><term>Insuline (pharmacologie)</term><term>Lignée cellulaire</term><term>Oligonucléotides antisens (métabolisme)</term><term>Oligonucléotides antisens (synthèse chimique)</term><term>Phosphatidyléthanolamine (pharmacologie)</term><term>Régions promotrices (génétique) ()</term><term>Séquence nucléotidique</term><term>Transfection</term><term>Transport biologique ()</term><term>Tumeurs du côlon</term></keywords><keywords scheme="MESH" type="chemical" qualifier="biosynthesis" xml:lang="en"><term>Transforming Growth Factor alpha</term></keywords><keywords scheme="MESH" type="chemical" qualifier="chemical synthesis" xml:lang="en"><term>Oligonucleotides, Antisense</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Chloramphenicol O-Acetyltransferase</term><term>Transforming Growth Factor alpha</term></keywords><keywords scheme="MESH" qualifier="biosynthèse" xml:lang="fr"><term>Facteur de croissance transformant alpha</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Biological Transport</term><term>Cell Division</term><term>Promoter Regions, Genetic</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Chloramphenicol O-acetyltransferase</term><term>Facteur de croissance transformant alpha</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Chloramphenicol O-Acetyltransferase</term><term>DNA, Antisense</term><term>Oligonucleotides, Antisense</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>ADN antisens</term><term>Chloramphenicol O-acetyltransferase</term><term>Oligonucléotides antisens</term></keywords><keywords scheme="MESH" 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It was found that tumor cell growth was inhibited when HCT116 cells were treated with Lipofectin-DNA oligomer complexes or with Lipofectin alone. Uptake of 32P-labeled 15-mers into colon tumor cells was compared in the presence and absence of Lipofectin. The amount of labeled oligomer found in cells that received optimal ratios of Lipofectin to DNA was 4- to 10-fold higher than the amount found in cells that received 32P-labeled DNA alone. Although Lipofectin-antisense DNA oligomer treatment of HCT116 cells caused a dose-dependent inhibition of cell growth, there was a subsequent rise in target mRNA product. Because the mechanism of growth inhibition could not involve an inhibition of TGF-alpha expression, it was concluded that Lipofectin probably exerts a nonspecific, detergent-like effect upon the cell membrane, producing an enhancement of TGF-alpha processing and release.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">1422086</PMID><DateCompleted><Year>1992</Year><Month>12</Month><Day>08</Day></DateCompleted><DateRevised><Year>2019</Year><Month>10</Month><Day>28</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">1050-5261</ISSN><JournalIssue CitedMedium="Print"><Volume>2</Volume><Issue>1</Issue><PubDate><Year>1992</Year><Season>Spring</Season></PubDate></JournalIssue><Title>Antisense research and development</Title><ISOAbbreviation>Antisense Res. Dev.</ISOAbbreviation></Journal><ArticleTitle>Lipofectin enhances cellular uptake of antisense DNA while inhibiting tumor cell growth.</ArticleTitle><Pagination><MedlinePgn>51-9</MedlinePgn></Pagination><Abstract><AbstractText>A natural DNA oligomer (15-mer) was synthesized with a sequence complementary to the translation initiation codon region of the human TGF-alpha mRNA and mixed with Lipofectin to form unilamellar complexes. It was found that tumor cell growth was inhibited when HCT116 cells were treated with Lipofectin-DNA oligomer complexes or with Lipofectin alone. Uptake of 32P-labeled 15-mers into colon tumor cells was compared in the presence and absence of Lipofectin. The amount of labeled oligomer found in cells that received optimal ratios of Lipofectin to DNA was 4- to 10-fold higher than the amount found in cells that received 32P-labeled DNA alone. Although Lipofectin-antisense DNA oligomer treatment of HCT116 cells caused a dose-dependent inhibition of cell growth, there was a subsequent rise in target mRNA product. Because the mechanism of growth inhibition could not involve an inhibition of TGF-alpha expression, it was concluded that Lipofectin probably exerts a nonspecific, detergent-like effect upon the cell membrane, producing an enhancement of TGF-alpha processing and release.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Yeoman</LastName><ForeName>L C</ForeName><Initials>LC</Initials><AffiliationInfo><Affiliation>Department of Pharmacology, Baylor College of Medicine, Houston, Texas.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Danels</LastName><ForeName>Y J</ForeName><Initials>YJ</Initials></Author><Author ValidYN="Y"><LastName>Lynch</LastName><ForeName>M J</ForeName><Initials>MJ</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>CA45967</GrantID><Acronym>CA</Acronym><Agency>NCI NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType><PublicationType UI="D013487">Research Support, U.S. Gov't, P.H.S.</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Antisense Res Dev</MedlineTA><NlmUniqueID>9110698</NlmUniqueID><ISSNLinking>1050-5261</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D016373">DNA, Antisense</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D007328">Insulin</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D016376">Oligonucleotides, Antisense</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D010714">Phosphatidylethanolamines</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance 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effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002460" MajorTopicYN="N">Cell Line</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015500" MajorTopicYN="N">Chloramphenicol O-Acetyltransferase</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003110" MajorTopicYN="N">Colonic Neoplasms</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016373" MajorTopicYN="N">DNA, Antisense</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004815" MajorTopicYN="N">Epidermal Growth Factor</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007328" MajorTopicYN="N">Insulin</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007700" MajorTopicYN="N">Kinetics</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008969" MajorTopicYN="N">Molecular Sequence Data</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016376" MajorTopicYN="N">Oligonucleotides, Antisense</DescriptorName><QualifierName UI="Q000138" MajorTopicYN="N">chemical synthesis</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010714" MajorTopicYN="N">Phosphatidylethanolamines</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011401" MajorTopicYN="N">Promoter Regions, Genetic</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="Y">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D014162" MajorTopicYN="N">Transfection</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016211" MajorTopicYN="N">Transforming Growth Factor alpha</DescriptorName><QualifierName UI="Q000096" MajorTopicYN="N">biosynthesis</QualifierName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D014407" MajorTopicYN="N">Tumor Cells, Cultured</DescriptorName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>1992</Year><Month>1</Month><Day>1</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>1992</Year><Month>1</Month><Day>1</Day><Hour>0</Hour><Minute>1</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>1992</Year><Month>1</Month><Day>1</Day><Hour>0</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">1422086</ArticleId><ArticleId IdType="doi">10.1089/ard.1992.2.51</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>États-Unis</li></country><region><li>Texas</li></region></list><tree><noCountry><name sortKey="Danels, Y J" sort="Danels, Y J" uniqKey="Danels Y" first="Y J" last="Danels">Y J Danels</name><name sortKey="Lynch, M J" sort="Lynch, M J" uniqKey="Lynch M" first="M J" last="Lynch">M J Lynch</name></noCountry><country name="États-Unis"><region name="Texas"><name sortKey="Yeoman, L C" sort="Yeoman, L C" uniqKey="Yeoman L" first="L C" last="Yeoman">L C Yeoman</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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