Transduction effect of antisense K-ras on malignant phenotypes in gastric cancer cells
Identifieur interne : 001626 ( Istex/Corpus ); précédent : 001625; suivant : 001627Transduction effect of antisense K-ras on malignant phenotypes in gastric cancer cells
Auteurs : Jae J. Song ; Heuiran Lee ; Eunhee Kim ; Yeon S. Kim ; Nae C. Yoo ; Jae K. Roh ; Byung S. Kim ; Joohang KimSource :
- Cancer Letters [ 0304-3835 ] ; 2000.
English descriptors
- KwdEn :
- Teeft :
- Abdominal wall, Aberrant expression, Amersham pharmacia, Antisense, Antisense oligonucleotides, Antitumoral effects, Cancer cell lines, Cancer cells, Cancer letters, Cells transduced, Codon, Control group, Direct nucleotide sequencing, Direct sequencing analysis, Elsevier science ireland, Exon, Experimental group, Expression level, Expression levels, Gastric, Gastric cancer, Gastric cancer cell lines, Gastric cancer cells, Gastric cells, Genomic, Genomic dnas, Growth inhibition, Growth rate, Homozygous mutation, Human cancers, Human pancreatic cancer cell lines, Immunoblotting, Immunoblotting analysis, Initial mass, Korea research institute, Lncx, Lung cancer cells, Lysis buffer, Mutation, Neomycin phosphotransferase gene, Parental lane, Point mutation, Point mutations, Polymerase chain strand conformation polymorphism, Primer, Product sequencing, Recombinant retrovirus, Reduction rate, Retroviral vector, Retrovirus, Santa cruz, Sequencing, Sequencing primer, Several reports, Third exons, Transduced, Transduced cells, Tumor volume, Tumorigenicity, Wild type, Wild type gene, Yonsei cancer center, Yonsei university college.
Abstract
Abstract: The antitumoral effects of antisense RNA to K-ras were investigated in gastric cancer cell lines by examining the level of K-ras expression and the tumorigenicity in vitro and in vivo. Polymerase chain reaction-single strand conformation polymorphism (PCR-SSCP), DNA sequencing, and immunoblotting analysis revealed that YCC-1 gastric cancer cells overexpressed wild type K-ras, whereas YCC-2 cells had a homozygous mutation in codon 12 from GGT (glycine) to AGT (serine), while SNU-1 cells had a heterozygous mutation to GAT (asparagine) in the identical position. Both YCC-1 and YCC-2 cells were transduced by LNC-AS/K-ras containing the antisense 2.2 kb genomic K-ras DNA fragment covering exon 2 and exon 3 specific for K-ras. The application of antisense K-ras significantly downregulated the expression of K-ras and had no influence on the expression of either H-ras or N-ras. The antisense-transduced YCC-2 cells grew considerably slower than the control group transduced by LNCX, whereas the growth inhibition of antisense-transduced YCC-1 cells was less prominent than that of transduced YCC-2 cells. In addition, the tumorigenicity of YCC-2 cells transduced by LNC-AS/K-ras was totally lost. Therefore, our results imply that the specific inhibition of K-ras p21 protein can be accomplished by introducing the antisense covering the K-ras- specific region to gastric cancer cells with aberrant K-ras expression, resulting in a reduction of the growth rate and suppression of tumorigenicity.
Url:
DOI: 10.1016/S0304-3835(00)00417-1
Links to Exploration step
ISTEX:C81FFCF7831BDD96949F7A8CA6B5005A89E7B4A6Le document en format XML
<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title xml:lang="en">Transduction effect of antisense K-ras on malignant phenotypes in gastric cancer cells</title><author><name sortKey="Song, Jae J" sort="Song, Jae J" uniqKey="Song J" first="Jae J" last="Song">Jae J. Song</name><affiliation><mods:affiliation>Institute for Cancer Research, Yonsei University College of Medicine, Yonsei Cancer Center, Seoul, 120 752, South Korea</mods:affiliation></affiliation></author><author><name sortKey="Lee, Heuiran" sort="Lee, Heuiran" uniqKey="Lee H" first="Heuiran" last="Lee">Heuiran Lee</name><affiliation><mods:affiliation>Department of Microbiology, University of Ulsan, College of Medicine, Ulsan, South Korea</mods:affiliation></affiliation></author><author><name sortKey="Kim, Eunhee" sort="Kim, Eunhee" uniqKey="Kim E" first="Eunhee" last="Kim">Eunhee Kim</name><affiliation><mods:affiliation>Institute for Cancer Research, Yonsei University College of Medicine, Yonsei Cancer Center, Seoul, 120 752, South Korea</mods:affiliation></affiliation></author><author><name sortKey="Kim, Yeon S" sort="Kim, Yeon S" uniqKey="Kim Y" first="Yeon S" last="Kim">Yeon S. Kim</name><affiliation><mods:affiliation>Korea Research Institute of Bioscience & Technology, Seoul, South Korea</mods:affiliation></affiliation></author><author><name sortKey="Yoo, Nae C" sort="Yoo, Nae C" uniqKey="Yoo N" first="Nae C" last="Yoo">Nae C. Yoo</name><affiliation><mods:affiliation>Institute for Cancer Research, Yonsei University College of Medicine, Yonsei Cancer Center, Seoul, 120 752, South Korea</mods:affiliation></affiliation><affiliation><mods:affiliation>Yonsei Cancer Center, Yonsei University College of Medicine, Seoul, South Korea</mods:affiliation></affiliation></author><author><name sortKey="Roh, Jae K" sort="Roh, Jae K" uniqKey="Roh J" first="Jae K" last="Roh">Jae K. Roh</name><affiliation><mods:affiliation>Institute for Cancer Research, Yonsei University College of Medicine, Yonsei Cancer Center, Seoul, 120 752, South Korea</mods:affiliation></affiliation><affiliation><mods:affiliation>Yonsei Cancer Center, Yonsei University College of Medicine, Seoul, South Korea</mods:affiliation></affiliation></author><author><name sortKey="Kim, Byung S" sort="Kim, Byung S" uniqKey="Kim B" first="Byung S" last="Kim">Byung S. Kim</name><affiliation><mods:affiliation>Institute for Cancer Research, Yonsei University College of Medicine, Yonsei Cancer Center, Seoul, 120 752, South Korea</mods:affiliation></affiliation><affiliation><mods:affiliation>Yonsei Cancer Center, Yonsei University College of Medicine, Seoul, South Korea</mods:affiliation></affiliation></author><author><name sortKey="Kim, Joohang" sort="Kim, Joohang" uniqKey="Kim J" first="Joohang" last="Kim">Joohang Kim</name><affiliation><mods:affiliation>Institute for Cancer Research, Yonsei University College of Medicine, Yonsei Cancer Center, Seoul, 120 752, South Korea</mods:affiliation></affiliation><affiliation><mods:affiliation>Yonsei Cancer Center, Yonsei University College of Medicine, Seoul, South Korea</mods:affiliation></affiliation><affiliation><mods:affiliation>Corresponding author. Tel.: +82-2-361-7622; fax: + 82-2-392-1508</mods:affiliation></affiliation><affiliation><mods:affiliation>E-mail: kjhang@yumc.yonsei.ac.kr</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:C81FFCF7831BDD96949F7A8CA6B5005A89E7B4A6</idno><date when="2000" year="2000">2000</date><idno type="doi">10.1016/S0304-3835(00)00417-1</idno><idno type="url">https://api.istex.fr/ark:/67375/6H6-JDGR89P1-V/fulltext.pdf</idno><idno type="wicri:Area/Istex/Corpus">001626</idno><idno type="wicri:explorRef" wicri:stream="Istex" wicri:step="Corpus" wicri:corpus="ISTEX">001626</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">Transduction effect of antisense K-ras on malignant phenotypes in gastric cancer cells</title><author><name sortKey="Song, Jae J" sort="Song, Jae J" uniqKey="Song J" first="Jae J" last="Song">Jae J. Song</name><affiliation><mods:affiliation>Institute for Cancer Research, Yonsei University College of Medicine, Yonsei Cancer Center, Seoul, 120 752, South Korea</mods:affiliation></affiliation></author><author><name sortKey="Lee, Heuiran" sort="Lee, Heuiran" uniqKey="Lee H" first="Heuiran" last="Lee">Heuiran Lee</name><affiliation><mods:affiliation>Department of Microbiology, University of Ulsan, College of Medicine, Ulsan, South Korea</mods:affiliation></affiliation></author><author><name sortKey="Kim, Eunhee" sort="Kim, Eunhee" uniqKey="Kim E" first="Eunhee" last="Kim">Eunhee Kim</name><affiliation><mods:affiliation>Institute for Cancer Research, Yonsei University College of Medicine, Yonsei Cancer Center, Seoul, 120 752, South Korea</mods:affiliation></affiliation></author><author><name sortKey="Kim, Yeon S" sort="Kim, Yeon S" uniqKey="Kim Y" first="Yeon S" last="Kim">Yeon S. Kim</name><affiliation><mods:affiliation>Korea Research Institute of Bioscience & Technology, Seoul, South Korea</mods:affiliation></affiliation></author><author><name sortKey="Yoo, Nae C" sort="Yoo, Nae C" uniqKey="Yoo N" first="Nae C" last="Yoo">Nae C. Yoo</name><affiliation><mods:affiliation>Institute for Cancer Research, Yonsei University College of Medicine, Yonsei Cancer Center, Seoul, 120 752, South Korea</mods:affiliation></affiliation><affiliation><mods:affiliation>Yonsei Cancer Center, Yonsei University College of Medicine, Seoul, South Korea</mods:affiliation></affiliation></author><author><name sortKey="Roh, Jae K" sort="Roh, Jae K" uniqKey="Roh J" first="Jae K" last="Roh">Jae K. Roh</name><affiliation><mods:affiliation>Institute for Cancer Research, Yonsei University College of Medicine, Yonsei Cancer Center, Seoul, 120 752, South Korea</mods:affiliation></affiliation><affiliation><mods:affiliation>Yonsei Cancer Center, Yonsei University College of Medicine, Seoul, South Korea</mods:affiliation></affiliation></author><author><name sortKey="Kim, Byung S" sort="Kim, Byung S" uniqKey="Kim B" first="Byung S" last="Kim">Byung S. Kim</name><affiliation><mods:affiliation>Institute for Cancer Research, Yonsei University College of Medicine, Yonsei Cancer Center, Seoul, 120 752, South Korea</mods:affiliation></affiliation><affiliation><mods:affiliation>Yonsei Cancer Center, Yonsei University College of Medicine, Seoul, South Korea</mods:affiliation></affiliation></author><author><name sortKey="Kim, Joohang" sort="Kim, Joohang" uniqKey="Kim J" first="Joohang" last="Kim">Joohang Kim</name><affiliation><mods:affiliation>Institute for Cancer Research, Yonsei University College of Medicine, Yonsei Cancer Center, Seoul, 120 752, South Korea</mods:affiliation></affiliation><affiliation><mods:affiliation>Yonsei Cancer Center, Yonsei University College of Medicine, Seoul, South Korea</mods:affiliation></affiliation><affiliation><mods:affiliation>Corresponding author. Tel.: +82-2-361-7622; fax: + 82-2-392-1508</mods:affiliation></affiliation><affiliation><mods:affiliation>E-mail: kjhang@yumc.yonsei.ac.kr</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Cancer Letters</title><title level="j" type="abbrev">CAN</title><idno type="ISSN">0304-3835</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="2000">2000</date><biblScope unit="volume">157</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="1">1</biblScope><biblScope unit="page" to="7">7</biblScope></imprint><idno type="ISSN">0304-3835</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0304-3835</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Antisense</term><term>Gastric cancer</term><term>Gene therapy</term><term>K-ras</term></keywords><keywords scheme="Teeft" xml:lang="en"><term>Abdominal wall</term><term>Aberrant expression</term><term>Amersham pharmacia</term><term>Antisense</term><term>Antisense oligonucleotides</term><term>Antitumoral effects</term><term>Cancer cell lines</term><term>Cancer cells</term><term>Cancer letters</term><term>Cells transduced</term><term>Codon</term><term>Control group</term><term>Direct nucleotide sequencing</term><term>Direct sequencing analysis</term><term>Elsevier science ireland</term><term>Exon</term><term>Experimental group</term><term>Expression level</term><term>Expression levels</term><term>Gastric</term><term>Gastric cancer</term><term>Gastric cancer cell lines</term><term>Gastric cancer cells</term><term>Gastric cells</term><term>Genomic</term><term>Genomic dnas</term><term>Growth inhibition</term><term>Growth rate</term><term>Homozygous mutation</term><term>Human cancers</term><term>Human pancreatic cancer cell lines</term><term>Immunoblotting</term><term>Immunoblotting analysis</term><term>Initial mass</term><term>Korea research institute</term><term>Lncx</term><term>Lung cancer cells</term><term>Lysis buffer</term><term>Mutation</term><term>Neomycin phosphotransferase gene</term><term>Parental lane</term><term>Point mutation</term><term>Point mutations</term><term>Polymerase chain strand conformation polymorphism</term><term>Primer</term><term>Product sequencing</term><term>Recombinant retrovirus</term><term>Reduction rate</term><term>Retroviral vector</term><term>Retrovirus</term><term>Santa cruz</term><term>Sequencing</term><term>Sequencing primer</term><term>Several reports</term><term>Third exons</term><term>Transduced</term><term>Transduced cells</term><term>Tumor volume</term><term>Tumorigenicity</term><term>Wild type</term><term>Wild type gene</term><term>Yonsei cancer center</term><term>Yonsei university college</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Abstract: The antitumoral effects of antisense RNA to K-ras were investigated in gastric cancer cell lines by examining the level of K-ras expression and the tumorigenicity in vitro and in vivo. Polymerase chain reaction-single strand conformation polymorphism (PCR-SSCP), DNA sequencing, and immunoblotting analysis revealed that YCC-1 gastric cancer cells overexpressed wild type K-ras, whereas YCC-2 cells had a homozygous mutation in codon 12 from GGT (glycine) to AGT (serine), while SNU-1 cells had a heterozygous mutation to GAT (asparagine) in the identical position. Both YCC-1 and YCC-2 cells were transduced by LNC-AS/K-ras containing the antisense 2.2 kb genomic K-ras DNA fragment covering exon 2 and exon 3 specific for K-ras. The application of antisense K-ras significantly downregulated the expression of K-ras and had no influence on the expression of either H-ras or N-ras. The antisense-transduced YCC-2 cells grew considerably slower than the control group transduced by LNCX, whereas the growth inhibition of antisense-transduced YCC-1 cells was less prominent than that of transduced YCC-2 cells. In addition, the tumorigenicity of YCC-2 cells transduced by LNC-AS/K-ras was totally lost. Therefore, our results imply that the specific inhibition of K-ras p21 protein can be accomplished by introducing the antisense covering the K-ras- specific region to gastric cancer cells with aberrant K-ras expression, resulting in a reduction of the growth rate and suppression of tumorigenicity.</div></front></TEI><istex><corpusName>elsevier</corpusName><keywords><teeft><json:string>antisense</json:string><json:string>gastric</json:string><json:string>transduced</json:string><json:string>primer</json:string><json:string>lncx</json:string><json:string>exon</json:string><json:string>mutation</json:string><json:string>tumorigenicity</json:string><json:string>sequencing</json:string><json:string>cancer cells</json:string><json:string>retrovirus</json:string><json:string>gastric cancer cells</json:string><json:string>growth rate</json:string><json:string>immunoblotting analysis</json:string><json:string>cancer 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college</json:string><json:string>direct nucleotide sequencing</json:string><json:string>sequencing primer</json:string><json:string>product sequencing</json:string><json:string>polymerase chain strand conformation polymorphism</json:string><json:string>third exons</json:string><json:string>point mutations</json:string><json:string>lysis buffer</json:string><json:string>human cancers</json:string><json:string>santa cruz</json:string><json:string>abdominal wall</json:string><json:string>tumor volume</json:string><json:string>direct sequencing analysis</json:string><json:string>several reports</json:string><json:string>genomic dnas</json:string><json:string>expression levels</json:string><json:string>gastric cells</json:string><json:string>korea research institute</json:string><json:string>point mutation</json:string><json:string>human pancreatic cancer cell lines</json:string><json:string>wild type gene</json:string><json:string>parental lane</json:string><json:string>elsevier science ireland</json:string><json:string>experimental group</json:string><json:string>initial mass</json:string><json:string>antisense oligonucleotides</json:string><json:string>lung cancer cells</json:string></teeft></keywords><author><json:item><name>Jae J Song</name><affiliations><json:string>Institute for Cancer Research, Yonsei University College of Medicine, Yonsei Cancer Center, Seoul, 120 752, South Korea</json:string></affiliations></json:item><json:item><name>Heuiran Lee</name><affiliations><json:string>Department of Microbiology, University of Ulsan, College of Medicine, Ulsan, South Korea</json:string></affiliations></json:item><json:item><name>Eunhee Kim</name><affiliations><json:string>Institute for Cancer Research, Yonsei University College of Medicine, Yonsei Cancer Center, Seoul, 120 752, South Korea</json:string></affiliations></json:item><json:item><name>Yeon S Kim</name><affiliations><json:string>Korea Research Institute of Bioscience & Technology, Seoul, South Korea</json:string></affiliations></json:item><json:item><name>Nae C Yoo</name><affiliations><json:string>Institute for Cancer Research, Yonsei University College of Medicine, Yonsei Cancer Center, Seoul, 120 752, South Korea</json:string><json:string>Yonsei Cancer Center, Yonsei University College of Medicine, Seoul, South Korea</json:string></affiliations></json:item><json:item><name>Jae K Roh</name><affiliations><json:string>Institute for Cancer Research, Yonsei University College of Medicine, Yonsei Cancer Center, Seoul, 120 752, South Korea</json:string><json:string>Yonsei Cancer Center, Yonsei University College of Medicine, Seoul, South Korea</json:string></affiliations></json:item><json:item><name>Byung S Kim</name><affiliations><json:string>Institute for Cancer Research, Yonsei University College of Medicine, Yonsei Cancer Center, Seoul, 120 752, South Korea</json:string><json:string>Yonsei Cancer Center, Yonsei University College of Medicine, Seoul, South Korea</json:string></affiliations></json:item><json:item><name>Joohang Kim</name><affiliations><json:string>Institute for Cancer Research, Yonsei University College of Medicine, Yonsei Cancer Center, Seoul, 120 752, South Korea</json:string><json:string>Yonsei Cancer Center, Yonsei University College of Medicine, Seoul, South Korea</json:string><json:string>Corresponding author. Tel.: +82-2-361-7622; fax: + 82-2-392-1508</json:string><json:string>E-mail: kjhang@yumc.yonsei.ac.kr</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>Gastric cancer</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>K-ras</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Antisense</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Gene therapy</value></json:item></subject><arkIstex>ark:/67375/6H6-JDGR89P1-V</arkIstex><language><json:string>eng</json:string></language><originalGenre><json:string>Short communication</json:string></originalGenre><abstract>Abstract: The antitumoral effects of antisense RNA to K-ras were investigated in gastric cancer cell lines by examining the level of K-ras expression and the tumorigenicity in vitro and in vivo. Polymerase chain reaction-single strand conformation polymorphism (PCR-SSCP), DNA sequencing, and immunoblotting analysis revealed that YCC-1 gastric cancer cells overexpressed wild type K-ras, whereas YCC-2 cells had a homozygous mutation in codon 12 from GGT (glycine) to AGT (serine), while SNU-1 cells had a heterozygous mutation to GAT (asparagine) in the identical position. Both YCC-1 and YCC-2 cells were transduced by LNC-AS/K-ras containing the antisense 2.2 kb genomic K-ras DNA fragment covering exon 2 and exon 3 specific for K-ras. The application of antisense K-ras significantly downregulated the expression of K-ras and had no influence on the expression of either H-ras or N-ras. The antisense-transduced YCC-2 cells grew considerably slower than the control group transduced by LNCX, whereas the growth inhibition of antisense-transduced YCC-1 cells was less prominent than that of transduced YCC-2 cells. In addition, the tumorigenicity of YCC-2 cells transduced by LNC-AS/K-ras was totally lost. Therefore, our results imply that the specific inhibition of K-ras p21 protein can be accomplished by introducing the antisense covering the K-ras- specific region to gastric cancer cells with aberrant K-ras expression, resulting in a reduction of the growth rate and suppression of tumorigenicity.</abstract><qualityIndicators><score>8.2</score><pdfWordCount>3548</pdfWordCount><pdfCharCount>21413</pdfCharCount><pdfVersion>1.2</pdfVersion><pdfPageCount>7</pdfPageCount><pdfPageSize>544 x 743 pts</pdfPageSize><refBibsNative>true</refBibsNative><abstractWordCount>221</abstractWordCount><abstractCharCount>1510</abstractCharCount><keywordCount>4</keywordCount></qualityIndicators><title>Transduction effect of antisense K-ras on malignant phenotypes in gastric cancer cells</title><pmid><json:string>10893435</json:string></pmid><pii><json:string>S0304-3835(00)00417-1</json:string></pii><genre><json:string>brief-communication</json:string></genre><host><title>Cancer Letters</title><language><json:string>unknown</json:string></language><publicationDate>2000</publicationDate><issn><json:string>0304-3835</json:string></issn><pii><json:string>S0304-3835(00)X0116-4</json:string></pii><volume>157</volume><issue>1</issue><pages><first>1</first><last>7</last></pages><genre><json:string>journal</json:string></genre></host><namedEntities><unitex><date><json:string>2000</json:string></date><geogName></geogName><orgName><json:string>Yonsei Cancer Center</json:string><json:string>Animal Research Committee Guidelines</json:string><json:string>Department of Microbiology, University of Ulsan, College of Medicine, Ulsan, South Korea</json:string><json:string>Yonsei University</json:string><json:string>Elsevier Science Ireland Ltd</json:string><json:string>Korea Research Institute of Bioscience</json:string><json:string>Korea Research Institute of Chemical Technology</json:string><json:string>Seoul National University</json:string><json:string>South Korea Received</json:string><json:string>Directed Research Fund of the Korea Research Foundation</json:string><json:string>Calbiochem, Cambridge</json:string></orgName><orgName_funder></orgName_funder><orgName_provider></orgName_provider><persName><json:string>H. Lee</json:string><json:string>J.J. Song</json:string></persName><placeName><json:string>Korea</json:string><json:string>Seoul</json:string><json:string>Valencia</json:string><json:string>Tumorigenicity</json:string><json:string>Santa Cruz</json:string><json:string>CA</json:string></placeName><ref_url></ref_url><ref_bibl><json:string>[18,22]</json:string><json:string>[4]</json:string><json:string>[23]</json:string><json:string>Kita et al.</json:string><json:string>[11]</json:string><json:string>[7,10,11]</json:string><json:string>[4,6,7]</json:string><json:string>[1]</json:string><json:string>[3,8,9]</json:string><json:string>[16]</json:string><json:string>J.J. Song et al.</json:string><json:string>[3,4]</json:string><json:string>[5]</json:string><json:string>[7]</json:string><json:string>[14]</json:string><json:string>Orita et al.</json:string><json:string>[2]</json:string><json:string>[16,17]</json:string></ref_bibl><bibl></bibl></unitex></namedEntities><ark><json:string>ark:/67375/6H6-JDGR89P1-V</json:string></ark><categories><wos><json:string>1 - science</json:string><json:string>2 - oncology</json:string></wos><scienceMetrix><json:string>1 - health sciences</json:string><json:string>2 - clinical medicine</json:string><json:string>3 - oncology & carcinogenesis</json:string></scienceMetrix><scopus><json:string>1 - Life Sciences</json:string><json:string>2 - Biochemistry, Genetics and Molecular Biology</json:string><json:string>3 - Cancer Research</json:string><json:string>1 - Health Sciences</json:string><json:string>2 - Medicine</json:string><json:string>3 - Oncology</json:string></scopus><inist><json:string>1 - sciences appliquees, technologies et medecines</json:string><json:string>2 - sciences biologiques et medicales</json:string><json:string>3 - sciences medicales</json:string></inist></categories><publicationDate>2000</publicationDate><copyrightDate>2000</copyrightDate><doi><json:string>10.1016/S0304-3835(00)00417-1</json:string></doi><id>C81FFCF7831BDD96949F7A8CA6B5005A89E7B4A6</id><score>1</score><fulltext><json:item><extension>pdf</extension><original>true</original><mimetype>application/pdf</mimetype><uri>https://api.istex.fr/ark:/67375/6H6-JDGR89P1-V/fulltext.pdf</uri></json:item><json:item><extension>zip</extension><original>false</original><mimetype>application/zip</mimetype><uri>https://api.istex.fr/ark:/67375/6H6-JDGR89P1-V/bundle.zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/ark:/67375/6H6-JDGR89P1-V/fulltext.tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">Transduction effect of antisense K-ras on malignant phenotypes in gastric cancer cells</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher scheme="https://scientific-publisher.data.istex.fr">ELSEVIER</publisher><availability><licence><p>©2000 Elsevier Science Ireland Ltd</p></licence><p scheme="https://loaded-corpus.data.istex.fr/ark:/67375/XBH-HKKZVM7B-M">elsevier</p></availability><date>2000</date></publicationStmt><notesStmt><note type="brief-communication" scheme="https://content-type.data.istex.fr/ark:/67375/XTP-S9SX2MFS-0">brief-communication</note><note type="journal" scheme="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">journal</note><note type="content">Fig. 1: (A) Single strand conformation polymorphism analysis of c-K-ras exon 1. Genomic DNAs were isolated from nine different gastric cancer cell lines and PCR was carried out with 5′ end-labeled primers specific to exon 1 or 2 of K-ras. PCR products were then separated on 6% non-denaturing polyacrylamide gel to detect the abnormal band mobilities. The PCR fragment containing exon 1 of YCC-2 only showed the abnormal band mobility as indicated by an arrow. (B) DNA sequencing analysis of YCC-2 and SNU-1 in c-K-ras exon 1 PCR products. The PCR products were sequenced with 5′ end-labeled sequencing primer using the PCR product sequencing kit.</note><note type="content">Fig. 2: (A) PCR analysis of YCC-1 and 2 cells transduced by retroviral vector. The genomic DNAs of parental YCC-1, 2 were extracted and PCR was carried out with primers specific to neomycin phosphotransferase gene. Lane 1, LNCX as a positive control; lane 2, parental YCC-1; lane 3, YCC-1 with LNCX; lane 4, YCC-1 with LNC-AS/K-ras; lane 5, parental YCC-2; lane 6, YCC-2 with LNCX; lane 7, YCC-2 with LNC-AS/K-ras. B. Immunoblotting analysis of ras p21 proteins in transduced YCC-1, 2 cells. Cells were lysed in lysis buffer and the cell lysates corresponding to 2.5×105 cells, except YCC-1 for K-ras (5×104) were loaded on 12% SDS-polyacrylamide as indicated by the expression level of α-actin. Proteins were transferred onto polyvinylidene difluoride membranes (PVDF) and probed with α-actin and ras-specific monoclonal antibodies. Lane 1, YCC-1 with LNCX; lane 2, YCC-1 with LNC-AS/K-ras; lane 3, YCC-2 with LNCX; lane 4, YCC-2 with LNC-AS/K-ras.</note><note type="content">Fig. 3: Growth curve of transduced gastric cancer cells. Transduced gastric cancer cells (1×103) were seeded in 48-well plates, harvested and counted by a hemocytometer at 24 h intervals. (A) Transduced YCC-1 cells. (B) Transduced YCC-2 cells.</note><note type="content">Fig. 4: Tumorigenicity of YCC-2 cells transduced with LNC-AS/K-ras in nu/nu mice. The nude mice (six animals per each group) were injected subcutaneously in the abdominal wall with 1×107 transduced YCC-2 cells and tumors were measured with a caliper at the indicated times. (A) Changes in tumor volume. (B) Photographs 2 months postimplantation of nu/nu mice implanted with YCC-2/LNCX as a control group (upper) and with LNC-AS/K-ras cells (lower).</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Transduction effect of antisense K-ras on malignant phenotypes in gastric cancer cells</title><author xml:id="author-0000"><persName><forename type="first">Jae J</forename><surname>Song</surname></persName><affiliation>Institute for Cancer Research, Yonsei University College of Medicine, Yonsei Cancer Center, Seoul, 120 752, South Korea</affiliation></author><author xml:id="author-0001"><persName><forename type="first">Heuiran</forename><surname>Lee</surname></persName><affiliation>Department of Microbiology, University of Ulsan, College of Medicine, Ulsan, South Korea</affiliation></author><author xml:id="author-0002"><persName><forename type="first">Eunhee</forename><surname>Kim</surname></persName><affiliation>Institute for Cancer Research, Yonsei University College of Medicine, Yonsei Cancer Center, Seoul, 120 752, South Korea</affiliation></author><author xml:id="author-0003"><persName><forename type="first">Yeon S</forename><surname>Kim</surname></persName><affiliation>Korea Research Institute of Bioscience & Technology, Seoul, South Korea</affiliation></author><author xml:id="author-0004"><persName><forename type="first">Nae C</forename><surname>Yoo</surname></persName><affiliation>Institute for Cancer Research, Yonsei University College of Medicine, Yonsei Cancer Center, Seoul, 120 752, South Korea</affiliation><affiliation>Yonsei Cancer Center, Yonsei University College of Medicine, Seoul, South Korea</affiliation></author><author xml:id="author-0005"><persName><forename type="first">Jae K</forename><surname>Roh</surname></persName><affiliation>Institute for Cancer Research, Yonsei University College of Medicine, Yonsei Cancer Center, Seoul, 120 752, South Korea</affiliation><affiliation>Yonsei Cancer Center, Yonsei University College of Medicine, Seoul, South Korea</affiliation></author><author xml:id="author-0006"><persName><forename type="first">Byung S</forename><surname>Kim</surname></persName><affiliation>Institute for Cancer Research, Yonsei University College of Medicine, Yonsei Cancer Center, Seoul, 120 752, South Korea</affiliation><affiliation>Yonsei Cancer Center, Yonsei University College of Medicine, Seoul, South Korea</affiliation></author><author xml:id="author-0007"><persName><forename type="first">Joohang</forename><surname>Kim</surname></persName><email>kjhang@yumc.yonsei.ac.kr</email><affiliation>Institute for Cancer Research, Yonsei University College of Medicine, Yonsei Cancer Center, Seoul, 120 752, South Korea</affiliation><affiliation>Yonsei Cancer Center, Yonsei University College of Medicine, Seoul, South Korea</affiliation><affiliation>Corresponding author. Tel.: +82-2-361-7622; fax: + 82-2-392-1508</affiliation></author><idno type="istex">C81FFCF7831BDD96949F7A8CA6B5005A89E7B4A6</idno><idno type="ark">ark:/67375/6H6-JDGR89P1-V</idno><idno type="DOI">10.1016/S0304-3835(00)00417-1</idno><idno type="PII">S0304-3835(00)00417-1</idno></analytic><monogr><title level="j">Cancer Letters</title><title level="j" type="abbrev">CAN</title><idno type="pISSN">0304-3835</idno><idno type="PII">S0304-3835(00)X0116-4</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="2000"></date><biblScope unit="volume">157</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="1">1</biblScope><biblScope unit="page" to="7">7</biblScope></imprint></monogr></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2000</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Abstract: The antitumoral effects of antisense RNA to K-ras were investigated in gastric cancer cell lines by examining the level of K-ras expression and the tumorigenicity in vitro and in vivo. Polymerase chain reaction-single strand conformation polymorphism (PCR-SSCP), DNA sequencing, and immunoblotting analysis revealed that YCC-1 gastric cancer cells overexpressed wild type K-ras, whereas YCC-2 cells had a homozygous mutation in codon 12 from GGT (glycine) to AGT (serine), while SNU-1 cells had a heterozygous mutation to GAT (asparagine) in the identical position. Both YCC-1 and YCC-2 cells were transduced by LNC-AS/K-ras containing the antisense 2.2 kb genomic K-ras DNA fragment covering exon 2 and exon 3 specific for K-ras. The application of antisense K-ras significantly downregulated the expression of K-ras and had no influence on the expression of either H-ras or N-ras. The antisense-transduced YCC-2 cells grew considerably slower than the control group transduced by LNCX, whereas the growth inhibition of antisense-transduced YCC-1 cells was less prominent than that of transduced YCC-2 cells. In addition, the tumorigenicity of YCC-2 cells transduced by LNC-AS/K-ras was totally lost. Therefore, our results imply that the specific inhibition of K-ras p21 protein can be accomplished by introducing the antisense covering the K-ras- specific region to gastric cancer cells with aberrant K-ras expression, resulting in a reduction of the growth rate and suppression of tumorigenicity.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>Gastric cancer</term></item><item><term>K-ras</term></item><item><term>Antisense</term></item><item><term>Gene therapy</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2000-02-01">Modified</change><change when="2000">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/ark:/67375/6H6-JDGR89P1-V/fulltext.txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Elsevier, elements deleted: ce:floats; body; tail"><istex:xmlDeclaration>version="1.0" encoding="utf-8"</istex:xmlDeclaration><istex:docType PUBLIC="-//ES//DTD journal article DTD version 4.5.2//EN//XML" URI="art452.dtd" name="istex:docType"><istex:entity SYSTEM="gr1" NDATA="IMAGE" name="gr1"></istex:entity><istex:entity SYSTEM="gr2" NDATA="IMAGE" name="gr2"></istex:entity><istex:entity SYSTEM="gr3" NDATA="IMAGE" name="gr3"></istex:entity><istex:entity SYSTEM="gr4" NDATA="IMAGE" name="gr4"></istex:entity></istex:docType><istex:document><converted-article version="4.5.2" docsubtype="sco" xml:lang="en"><item-info><jid>CAN</jid><aid>6005</aid><ce:pii>S0304-3835(00)00417-1</ce:pii><ce:doi>10.1016/S0304-3835(00)00417-1</ce:doi><ce:copyright type="full-transfer" year="2000">Elsevier Science Ireland Ltd</ce:copyright></item-info><head><ce:title>Transduction effect of antisense K-ras on malignant phenotypes in gastric cancer cells</ce:title><ce:author-group><ce:author><ce:given-name>Jae J</ce:given-name><ce:surname>Song</ce:surname><ce:cross-ref refid="AFF1"><ce:sup>a</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Heuiran</ce:given-name><ce:surname>Lee</ce:surname><ce:cross-ref refid="AFF2"><ce:sup>b</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Eunhee</ce:given-name><ce:surname>Kim</ce:surname><ce:cross-ref refid="AFF1"><ce:sup>a</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Yeon S</ce:given-name><ce:surname>Kim</ce:surname><ce:cross-ref refid="AFF3"><ce:sup>c</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Nae C</ce:given-name><ce:surname>Yoo</ce:surname><ce:cross-ref refid="AFF1"><ce:sup>a</ce:sup></ce:cross-ref><ce:cross-ref refid="AFF4"><ce:sup>d</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Jae K</ce:given-name><ce:surname>Roh</ce:surname><ce:cross-ref refid="AFF1"><ce:sup>a</ce:sup></ce:cross-ref><ce:cross-ref refid="AFF4"><ce:sup>d</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Byung S</ce:given-name><ce:surname>Kim</ce:surname><ce:cross-ref refid="AFF1"><ce:sup>a</ce:sup></ce:cross-ref><ce:cross-ref refid="AFF4"><ce:sup>d</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Joohang</ce:given-name><ce:surname>Kim</ce:surname><ce:cross-ref refid="AFF1"><ce:sup>a</ce:sup></ce:cross-ref><ce:cross-ref refid="AFF4"><ce:sup>d</ce:sup></ce:cross-ref><ce:cross-ref refid="CORR1">*</ce:cross-ref><ce:e-address>kjhang@yumc.yonsei.ac.kr</ce:e-address></ce:author><ce:affiliation id="AFF1"><ce:label>a</ce:label><ce:textfn>Institute for Cancer Research, Yonsei University College of Medicine, Yonsei Cancer Center, Seoul, 120 752, South Korea</ce:textfn></ce:affiliation><ce:affiliation id="AFF2"><ce:label>b</ce:label><ce:textfn>Department of Microbiology, University of Ulsan, College of Medicine, Ulsan, South Korea</ce:textfn></ce:affiliation><ce:affiliation id="AFF3"><ce:label>c</ce:label><ce:textfn>Korea Research Institute of Bioscience & Technology, Seoul, South Korea</ce:textfn></ce:affiliation><ce:affiliation id="AFF4"><ce:label>d</ce:label><ce:textfn>Yonsei Cancer Center, Yonsei University College of Medicine, Seoul, South Korea</ce:textfn></ce:affiliation><ce:correspondence id="CORR1"><ce:label>*</ce:label><ce:text>Corresponding author. Tel.: +82-2-361-7622; fax: + 82-2-392-1508</ce:text></ce:correspondence></ce:author-group><ce:date-received day="6" month="12" year="1999"></ce:date-received><ce:date-revised day="1" month="2" year="2000"></ce:date-revised><ce:date-accepted day="24" month="2" year="2000"></ce:date-accepted><ce:abstract><ce:section-title>Abstract</ce:section-title><ce:abstract-sec><ce:simple-para>The antitumoral effects of antisense RNA to K-ras were investigated in gastric cancer cell lines by examining the level of K-ras expression and the tumorigenicity in vitro and in vivo. Polymerase chain reaction-single strand conformation polymorphism (PCR-SSCP), DNA sequencing, and immunoblotting analysis revealed that YCC-1 gastric cancer cells overexpressed wild type K-ras, whereas YCC-2 cells had a homozygous mutation in codon 12 from GGT (glycine) to AGT (serine), while SNU-1 cells had a heterozygous mutation to GAT (asparagine) in the identical position. Both YCC-1 and YCC-2 cells were transduced by LNC-AS/K-ras containing the antisense 2.2 kb genomic K-ras DNA fragment covering exon 2 and exon 3 specific for K-ras. The application of antisense K-ras significantly downregulated the expression of K-ras and had no influence on the expression of either H-ras or N-ras. The antisense-transduced YCC-2 cells grew considerably slower than the control group transduced by LNCX, whereas the growth inhibition of antisense-transduced YCC-1 cells was less prominent than that of transduced YCC-2 cells. In addition, the tumorigenicity of YCC-2 cells transduced by LNC-AS/K-ras was totally lost. Therefore, our results imply that the specific inhibition of K-ras p21 protein can be accomplished by introducing the antisense covering the K-ras- specific region to gastric cancer cells with aberrant K-ras expression, resulting in a reduction of the growth rate and suppression of tumorigenicity.</ce:simple-para></ce:abstract-sec></ce:abstract><ce:keywords class="keyword" xml:lang="en"><ce:section-title>Keywords</ce:section-title><ce:keyword><ce:text>Gastric cancer</ce:text></ce:keyword><ce:keyword><ce:text>K-ras</ce:text></ce:keyword><ce:keyword><ce:text>Antisense</ce:text></ce:keyword><ce:keyword><ce:text>Gene therapy</ce:text></ce:keyword></ce:keywords></head></converted-article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Transduction effect of antisense K-ras on malignant phenotypes in gastric cancer cells</title></titleInfo><titleInfo type="alternative" lang="en" contentType="CDATA"><title>Transduction effect of antisense K-ras on malignant phenotypes in gastric cancer cells</title></titleInfo><name type="personal"><namePart type="given">Jae J</namePart><namePart type="family">Song</namePart><affiliation>Institute for Cancer Research, Yonsei University College of Medicine, Yonsei Cancer Center, Seoul, 120 752, South Korea</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Heuiran</namePart><namePart type="family">Lee</namePart><affiliation>Department of Microbiology, University of Ulsan, College of Medicine, Ulsan, South Korea</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Eunhee</namePart><namePart type="family">Kim</namePart><affiliation>Institute for Cancer Research, Yonsei University College of Medicine, Yonsei Cancer Center, Seoul, 120 752, South Korea</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Yeon S</namePart><namePart type="family">Kim</namePart><affiliation>Korea Research Institute of Bioscience & Technology, Seoul, South Korea</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Nae C</namePart><namePart type="family">Yoo</namePart><affiliation>Institute for Cancer Research, Yonsei University College of Medicine, Yonsei Cancer Center, Seoul, 120 752, South Korea</affiliation><affiliation>Yonsei Cancer Center, Yonsei University College of Medicine, Seoul, South Korea</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Jae K</namePart><namePart type="family">Roh</namePart><affiliation>Institute for Cancer Research, Yonsei University College of Medicine, Yonsei Cancer Center, Seoul, 120 752, South Korea</affiliation><affiliation>Yonsei Cancer Center, Yonsei University College of Medicine, Seoul, South Korea</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Byung S</namePart><namePart type="family">Kim</namePart><affiliation>Institute for Cancer Research, Yonsei University College of Medicine, Yonsei Cancer Center, Seoul, 120 752, South Korea</affiliation><affiliation>Yonsei Cancer Center, Yonsei University College of Medicine, Seoul, South Korea</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Joohang</namePart><namePart type="family">Kim</namePart><affiliation>Institute for Cancer Research, Yonsei University College of Medicine, Yonsei Cancer Center, Seoul, 120 752, South Korea</affiliation><affiliation>Yonsei Cancer Center, Yonsei University College of Medicine, Seoul, South Korea</affiliation><affiliation>Corresponding author. Tel.: +82-2-361-7622; fax: + 82-2-392-1508</affiliation><affiliation>E-mail: kjhang@yumc.yonsei.ac.kr</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="brief-communication" displayLabel="Short communication" authority="ISTEX" authorityURI="https://content-type.data.istex.fr" valueURI="https://content-type.data.istex.fr/ark:/67375/XTP-S9SX2MFS-0">brief-communication</genre><originInfo><publisher>ELSEVIER</publisher><dateIssued encoding="w3cdtf">2000</dateIssued><dateModified encoding="w3cdtf">2000-02-01</dateModified><copyrightDate encoding="w3cdtf">2000</copyrightDate></originInfo><language><languageTerm type="code" authority="iso639-2b">eng</languageTerm><languageTerm type="code" authority="rfc3066">en</languageTerm></language><abstract lang="en">Abstract: The antitumoral effects of antisense RNA to K-ras were investigated in gastric cancer cell lines by examining the level of K-ras expression and the tumorigenicity in vitro and in vivo. Polymerase chain reaction-single strand conformation polymorphism (PCR-SSCP), DNA sequencing, and immunoblotting analysis revealed that YCC-1 gastric cancer cells overexpressed wild type K-ras, whereas YCC-2 cells had a homozygous mutation in codon 12 from GGT (glycine) to AGT (serine), while SNU-1 cells had a heterozygous mutation to GAT (asparagine) in the identical position. Both YCC-1 and YCC-2 cells were transduced by LNC-AS/K-ras containing the antisense 2.2 kb genomic K-ras DNA fragment covering exon 2 and exon 3 specific for K-ras. The application of antisense K-ras significantly downregulated the expression of K-ras and had no influence on the expression of either H-ras or N-ras. The antisense-transduced YCC-2 cells grew considerably slower than the control group transduced by LNCX, whereas the growth inhibition of antisense-transduced YCC-1 cells was less prominent than that of transduced YCC-2 cells. In addition, the tumorigenicity of YCC-2 cells transduced by LNC-AS/K-ras was totally lost. Therefore, our results imply that the specific inhibition of K-ras p21 protein can be accomplished by introducing the antisense covering the K-ras- specific region to gastric cancer cells with aberrant K-ras expression, resulting in a reduction of the growth rate and suppression of tumorigenicity.</abstract><note type="content">Fig. 1: (A) Single strand conformation polymorphism analysis of c-K-ras exon 1. Genomic DNAs were isolated from nine different gastric cancer cell lines and PCR was carried out with 5′ end-labeled primers specific to exon 1 or 2 of K-ras. PCR products were then separated on 6% non-denaturing polyacrylamide gel to detect the abnormal band mobilities. The PCR fragment containing exon 1 of YCC-2 only showed the abnormal band mobility as indicated by an arrow. (B) DNA sequencing analysis of YCC-2 and SNU-1 in c-K-ras exon 1 PCR products. The PCR products were sequenced with 5′ end-labeled sequencing primer using the PCR product sequencing kit.</note><note type="content">Fig. 2: (A) PCR analysis of YCC-1 and 2 cells transduced by retroviral vector. The genomic DNAs of parental YCC-1, 2 were extracted and PCR was carried out with primers specific to neomycin phosphotransferase gene. Lane 1, LNCX as a positive control; lane 2, parental YCC-1; lane 3, YCC-1 with LNCX; lane 4, YCC-1 with LNC-AS/K-ras; lane 5, parental YCC-2; lane 6, YCC-2 with LNCX; lane 7, YCC-2 with LNC-AS/K-ras. B. Immunoblotting analysis of ras p21 proteins in transduced YCC-1, 2 cells. Cells were lysed in lysis buffer and the cell lysates corresponding to 2.5×105 cells, except YCC-1 for K-ras (5×104) were loaded on 12% SDS-polyacrylamide as indicated by the expression level of α-actin. Proteins were transferred onto polyvinylidene difluoride membranes (PVDF) and probed with α-actin and ras-specific monoclonal antibodies. Lane 1, YCC-1 with LNCX; lane 2, YCC-1 with LNC-AS/K-ras; lane 3, YCC-2 with LNCX; lane 4, YCC-2 with LNC-AS/K-ras.</note><note type="content">Fig. 3: Growth curve of transduced gastric cancer cells. Transduced gastric cancer cells (1×103) were seeded in 48-well plates, harvested and counted by a hemocytometer at 24 h intervals. (A) Transduced YCC-1 cells. (B) Transduced YCC-2 cells.</note><note type="content">Fig. 4: Tumorigenicity of YCC-2 cells transduced with LNC-AS/K-ras in nu/nu mice. The nude mice (six animals per each group) were injected subcutaneously in the abdominal wall with 1×107 transduced YCC-2 cells and tumors were measured with a caliper at the indicated times. (A) Changes in tumor volume. (B) Photographs 2 months postimplantation of nu/nu mice implanted with YCC-2/LNCX as a control group (upper) and with LNC-AS/K-ras cells (lower).</note><subject lang="en"><genre>Keywords</genre><topic>Gastric cancer</topic><topic>K-ras</topic><topic>Antisense</topic><topic>Gene therapy</topic></subject><relatedItem type="host"><titleInfo><title>Cancer Letters</title></titleInfo><titleInfo type="abbreviated"><title>CAN</title></titleInfo><genre type="journal" authority="ISTEX" authorityURI="https://publication-type.data.istex.fr" valueURI="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">journal</genre><originInfo><publisher>ELSEVIER</publisher><dateIssued encoding="w3cdtf">2000</dateIssued></originInfo><identifier type="ISSN">0304-3835</identifier><identifier type="PII">S0304-3835(00)X0116-4</identifier><part><date>2000</date><detail type="volume"><number>157</number><caption>vol.</caption></detail><detail type="issue"><number>1</number><caption>no.</caption></detail><extent unit="issue-pages"><start>1</start><end>113</end></extent><extent unit="pages"><start>1</start><end>7</end></extent></part></relatedItem><identifier type="istex">C81FFCF7831BDD96949F7A8CA6B5005A89E7B4A6</identifier><identifier type="ark">ark:/67375/6H6-JDGR89P1-V</identifier><identifier type="DOI">10.1016/S0304-3835(00)00417-1</identifier><identifier type="PII">S0304-3835(00)00417-1</identifier><accessCondition type="use and reproduction" contentType="copyright">©2000 Elsevier Science Ireland Ltd</accessCondition><recordInfo><recordContentSource authority="ISTEX" authorityURI="https://loaded-corpus.data.istex.fr" valueURI="https://loaded-corpus.data.istex.fr/ark:/67375/XBH-HKKZVM7B-M">elsevier</recordContentSource><recordOrigin>Elsevier Science Ireland Ltd, ©2000</recordOrigin></recordInfo></mods><json:item><extension>json</extension><original>false</original><mimetype>application/json</mimetype><uri>https://api.istex.fr/ark:/67375/6H6-JDGR89P1-V/record.json</uri></json:item></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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