Rad51 siRNA delivered by HVJ envelope vector enhances the anti‐cancer effect of cisplatin
Identifieur interne : 001B41 ( Istex/Corpus ); précédent : 001B40; suivant : 001B42Rad51 siRNA delivered by HVJ envelope vector enhances the anti‐cancer effect of cisplatin
Auteurs : Makoto Ito ; Seiji Yamamoto ; Keisuke Nimura ; Kazuya Hiraoka ; Katsuto Tamai ; Yasufumi KanedaSource :
- The Journal of Gene Medicine [ 1099-498X ] ; 2005-08.
English descriptors
- Teeft :
- Antisense, Antisense oligonucleotides, Apoptosis, Biochem biophys, Cancer cell lines, Cancer cells, Cancer therapy, Cddp, Cddp conc, Cddp sensitivity, Cddp treatment, Cell lines, Cell number, Cisplatin, Copyright, Envelope vector, Hela, Hela cells, Hemagglutinating virus, Human cancer cells, Intraperitoneal injection, John wiley sons, Kaneda, Nhdf, Northern blot analysis, Oligonucleotides, Osaka university, Particle counter, Protein kinase, Protein level, Protein levels, Recombination, Relative cell count, Santa cruz, Scid mice, Similar results, Sirna, Sirna cddp, Sirna medium, Sirna transfer, Standard deviation, Synthetic sirna, Target protein, Transfection, Triplicate samples, Tumor growth, Tumor mass, Various concentrations, Western blot analysis.
Abstract
Background: Every cancer therapy appears to be transiently effective for cancer regression, but cancers gradually transform to be resistant to the therapy. Cancers also develop machineries to resist chemotherapy. Short interfering RNA (siRNA) has been evaluated as an attractive and effective tool for suppressing a target protein by specifically digesting its mRNA. Suppression of the machineries using siRNA may enhance the sensitivity to chemotherapy in cancers when combined with an effective delivery system. Methods: To enhance the anti‐cancer effect of chemotherapy, we transferred siRNA against Rad51 into various human cancer cells using the HVJ (hemagglutinating virus of Japan, Sendai virus) envelope vector in the presence or absence of cis‐diamminedichloroplatinum(II) (CDDP, cisplatin). The inhibition of cell growth was assessed by a modified MTT assay, counting cell number, or fluorescence‐activated cell sorting (FACS) analysis after Annexin V labeling. The synthetic Rad51 siRNA was also introduced into subcutaneous tumor masses of HeLa cells in SCID mice with or without intraperitoneal injection of CDDP, and tumor growth was monitored. Results: When synthetic Rad51 siRNA was delivered into HeLa cells using the HVJ envelope vector, no Rad51 transcripts were detected on day 2, and Rad51 protein completely disappeared for 4 days after siRNA transfer. When HeLa cells were incubated with 0.02 µg/ml CDDP for 3 h after siRNA transfer, the number of colonies decreased to approximately 10% of that with scrambled siRNA. The sensitivity to CDDP was enhanced in various human cancer cells, but not in normal human fibroblasts. When Rad51 siRNA was delivered into tumors using the HVJ envelope vector, the Rad51 transcript level was reduced to approximately 25%. Rad51 siRNA combined with CDDP significantly inhibited tumor growth when compared to siRNA or CDDP alone. Conclusions: Rad51 siRNA could enhance the sensitivity to CDDP in cancer cells both in vitro and in vivo. Our results suggest that the combination of CDDP and Rad51 siRNA will be an effective anti‐cancer protocol. Copyright © 2005 John Wiley & Sons, Ltd.
Url:
DOI: 10.1002/jgm.753
Links to Exploration step
ISTEX:5FBC2E8437334FEAA3AE96D3A2F6E063AD351F5DLe document en format XML
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Nimura</name><affiliation><mods:affiliation>Division of Gene Therapy Science, Graduate School of Medicine, Osaka University, 2‐2 Yamada‐oka, Suita, Osaka 565 ‐0871, Japan</mods:affiliation></affiliation></author><author><name sortKey="Hiraoka, Kazuya" sort="Hiraoka, Kazuya" uniqKey="Hiraoka K" first="Kazuya" last="Hiraoka">Kazuya Hiraoka</name><affiliation><mods:affiliation>Division of Gene Therapy Science, Graduate School of Medicine, Osaka University, 2‐2 Yamada‐oka, Suita, Osaka 565 ‐0871, Japan</mods:affiliation></affiliation></author><author><name sortKey="Tamai, Katsuto" sort="Tamai, Katsuto" uniqKey="Tamai K" first="Katsuto" last="Tamai">Katsuto Tamai</name><affiliation><mods:affiliation>Division of Gene Therapy Science, Graduate School of Medicine, Osaka University, 2‐2 Yamada‐oka, Suita, Osaka 565 ‐0871, Japan</mods:affiliation></affiliation></author><author><name sortKey="Kaneda, Yasufumi" sort="Kaneda, Yasufumi" uniqKey="Kaneda Y" first="Yasufumi" last="Kaneda">Yasufumi Kaneda</name><affiliation><mods:affiliation>Division of Gene Therapy Science, Graduate School of Medicine, Osaka University, 2‐2 Yamada‐oka, Suita, Osaka 565 ‐0871, Japan</mods:affiliation></affiliation><affiliation><mods:affiliation>E-mail: kaneday@gts.med.osaka‐u.ac.jp</mods:affiliation></affiliation><affiliation><mods:affiliation>Correspondence address: Division of Gene Therapy Science, Graduate School of Medicine, Osaka University, 2‐2 Yamada‐oka, Suita, Osaka 565‐0871, Japan.</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j" type="main">The Journal of Gene Medicine</title><title level="j" type="alt">JOURNAL OF GENE MEDICINE, THE</title><idno type="ISSN">1099-498X</idno><idno type="eISSN">1521-2254</idno><imprint><biblScope unit="vol">7</biblScope><biblScope unit="issue">8</biblScope><biblScope unit="page" from="1044">1044</biblScope><biblScope unit="page" to="1052">1052</biblScope><biblScope unit="page-count">9</biblScope><publisher>John Wiley & Sons, Ltd.</publisher><pubPlace>Chichester, UK</pubPlace><date type="published" when="2005-08">2005-08</date></imprint><idno type="ISSN">1099-498X</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">1099-498X</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="Teeft" xml:lang="en"><term>Antisense</term><term>Antisense oligonucleotides</term><term>Apoptosis</term><term>Biochem biophys</term><term>Cancer cell lines</term><term>Cancer cells</term><term>Cancer therapy</term><term>Cddp</term><term>Cddp conc</term><term>Cddp sensitivity</term><term>Cddp treatment</term><term>Cell lines</term><term>Cell number</term><term>Cisplatin</term><term>Copyright</term><term>Envelope vector</term><term>Hela</term><term>Hela cells</term><term>Hemagglutinating virus</term><term>Human cancer cells</term><term>Intraperitoneal injection</term><term>John wiley sons</term><term>Kaneda</term><term>Nhdf</term><term>Northern blot analysis</term><term>Oligonucleotides</term><term>Osaka university</term><term>Particle counter</term><term>Protein kinase</term><term>Protein level</term><term>Protein levels</term><term>Recombination</term><term>Relative cell count</term><term>Santa cruz</term><term>Scid mice</term><term>Similar results</term><term>Sirna</term><term>Sirna cddp</term><term>Sirna medium</term><term>Sirna transfer</term><term>Standard deviation</term><term>Synthetic sirna</term><term>Target protein</term><term>Transfection</term><term>Triplicate samples</term><term>Tumor growth</term><term>Tumor mass</term><term>Various concentrations</term><term>Western blot analysis</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Background: Every cancer therapy appears to be transiently effective for cancer regression, but cancers gradually transform to be resistant to the therapy. Cancers also develop machineries to resist chemotherapy. Short interfering RNA (siRNA) has been evaluated as an attractive and effective tool for suppressing a target protein by specifically digesting its mRNA. Suppression of the machineries using siRNA may enhance the sensitivity to chemotherapy in cancers when combined with an effective delivery system. Methods: To enhance the anti‐cancer effect of chemotherapy, we transferred siRNA against Rad51 into various human cancer cells using the HVJ (hemagglutinating virus of Japan, Sendai virus) envelope vector in the presence or absence of cis‐diamminedichloroplatinum(II) (CDDP, cisplatin). The inhibition of cell growth was assessed by a modified MTT assay, counting cell number, or fluorescence‐activated cell sorting (FACS) analysis after Annexin V labeling. The synthetic Rad51 siRNA was also introduced into subcutaneous tumor masses of HeLa cells in SCID mice with or without intraperitoneal injection of CDDP, and tumor growth was monitored. Results: When synthetic Rad51 siRNA was delivered into HeLa cells using the HVJ envelope vector, no Rad51 transcripts were detected on day 2, and Rad51 protein completely disappeared for 4 days after siRNA transfer. When HeLa cells were incubated with 0.02 µg/ml CDDP for 3 h after siRNA transfer, the number of colonies decreased to approximately 10% of that with scrambled siRNA. The sensitivity to CDDP was enhanced in various human cancer cells, but not in normal human fibroblasts. When Rad51 siRNA was delivered into tumors using the HVJ envelope vector, the Rad51 transcript level was reduced to approximately 25%. Rad51 siRNA combined with CDDP significantly inhibited tumor growth when compared to siRNA or CDDP alone. Conclusions: Rad51 siRNA could enhance the sensitivity to CDDP in cancer cells both in vitro and in vivo. Our results suggest that the combination of CDDP and Rad51 siRNA will be an effective anti‐cancer protocol. Copyright © 2005 John Wiley & Sons, Ltd.</div></front></TEI><istex><corpusName>wiley</corpusName><keywords><teeft><json:string>sirna</json:string><json:string>cddp</json:string><json:string>hela</json:string><json:string>envelope vector</json:string><json:string>hela cells</json:string><json:string>cisplatin</json:string><json:string>nhdf</json:string><json:string>antisense</json:string><json:string>john wiley sons</json:string><json:string>copyright</json:string><json:string>oligonucleotides</json:string><json:string>recombination</json:string><json:string>cancer cells</json:string><json:string>cddp sensitivity</json:string><json:string>apoptosis</json:string><json:string>transfection</json:string><json:string>kaneda</json:string><json:string>cell number</json:string><json:string>tumor growth</json:string><json:string>antisense oligonucleotides</json:string><json:string>cell lines</json:string><json:string>northern blot analysis</json:string><json:string>scid mice</json:string><json:string>cancer therapy</json:string><json:string>human cancer cells</json:string><json:string>intraperitoneal injection</json:string><json:string>sirna transfer</json:string><json:string>triplicate samples</json:string><json:string>sirna medium</json:string><json:string>cancer cell lines</json:string><json:string>particle counter</json:string><json:string>tumor mass</json:string><json:string>target protein</json:string><json:string>cddp treatment</json:string><json:string>protein kinase</json:string><json:string>cddp conc</json:string><json:string>various concentrations</json:string><json:string>osaka university</json:string><json:string>protein level</json:string><json:string>similar results</json:string><json:string>standard deviation</json:string><json:string>western blot analysis</json:string><json:string>protein levels</json:string><json:string>relative cell count</json:string><json:string>sirna cddp</json:string><json:string>hemagglutinating virus</json:string><json:string>santa cruz</json:string><json:string>synthetic sirna</json:string><json:string>biochem biophys</json:string></teeft></keywords><author><json:item><name>Makoto Ito</name><affiliations><json:string>Division of Gene Therapy Science, Graduate School of Medicine, Osaka University, 2‐2 Yamada‐oka, Suita, Osaka 565 ‐0871, Japan</json:string></affiliations></json:item><json:item><name>Seiji Yamamoto</name><affiliations><json:string>Division of Gene Therapy Science, Graduate School of Medicine, Osaka University, 2‐2 Yamada‐oka, Suita, Osaka 565 ‐0871, Japan</json:string></affiliations></json:item><json:item><name>Keisuke Nimura</name><affiliations><json:string>Division of Gene Therapy Science, Graduate School of Medicine, Osaka University, 2‐2 Yamada‐oka, Suita, Osaka 565 ‐0871, Japan</json:string></affiliations></json:item><json:item><name>Kazuya Hiraoka</name><affiliations><json:string>Division of Gene Therapy Science, Graduate School of Medicine, Osaka University, 2‐2 Yamada‐oka, Suita, Osaka 565 ‐0871, Japan</json:string></affiliations></json:item><json:item><name>Katsuto Tamai</name><affiliations><json:string>Division of Gene Therapy Science, Graduate School of Medicine, Osaka University, 2‐2 Yamada‐oka, Suita, Osaka 565 ‐0871, Japan</json:string></affiliations></json:item><json:item><name>Yasufumi Kaneda</name><affiliations><json:string>Division of Gene Therapy Science, Graduate School of Medicine, Osaka University, 2‐2 Yamada‐oka, Suita, Osaka 565 ‐0871, Japan</json:string><json:string>E-mail: kaneday@gts.med.osaka‐u.ac.jp</json:string><json:string>Correspondence address: Division of Gene Therapy Science, Graduate School of Medicine, Osaka University, 2‐2 Yamada‐oka, Suita, Osaka 565‐0871, Japan.</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>chemotherapy</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>siRNA</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Rad51</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>non‐viral vector</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>drug delivery</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>cancer therapy</value></json:item></subject><articleId><json:string>JGM753</json:string></articleId><arkIstex>ark:/67375/WNG-GLHFLM13-6</arkIstex><language><json:string>eng</json:string></language><originalGenre><json:string>article</json:string></originalGenre><abstract>Background: Every cancer therapy appears to be transiently effective for cancer regression, but cancers gradually transform to be resistant to the therapy. Cancers also develop machineries to resist chemotherapy. Short interfering RNA (siRNA) has been evaluated as an attractive and effective tool for suppressing a target protein by specifically digesting its mRNA. Suppression of the machineries using siRNA may enhance the sensitivity to chemotherapy in cancers when combined with an effective delivery system. Methods: To enhance the anti‐cancer effect of chemotherapy, we transferred siRNA against Rad51 into various human cancer cells using the HVJ (hemagglutinating virus of Japan, Sendai virus) envelope vector in the presence or absence of cis‐diamminedichloroplatinum(II) (CDDP, cisplatin). The inhibition of cell growth was assessed by a modified MTT assay, counting cell number, or fluorescence‐activated cell sorting (FACS) analysis after Annexin V labeling. The synthetic Rad51 siRNA was also introduced into subcutaneous tumor masses of HeLa cells in SCID mice with or without intraperitoneal injection of CDDP, and tumor growth was monitored. Results: When synthetic Rad51 siRNA was delivered into HeLa cells using the HVJ envelope vector, no Rad51 transcripts were detected on day 2, and Rad51 protein completely disappeared for 4 days after siRNA transfer. When HeLa cells were incubated with 0.02 µg/ml CDDP for 3 h after siRNA transfer, the number of colonies decreased to approximately 10% of that with scrambled siRNA. The sensitivity to CDDP was enhanced in various human cancer cells, but not in normal human fibroblasts. When Rad51 siRNA was delivered into tumors using the HVJ envelope vector, the Rad51 transcript level was reduced to approximately 25%. Rad51 siRNA combined with CDDP significantly inhibited tumor growth when compared to siRNA or CDDP alone. Conclusions: Rad51 siRNA could enhance the sensitivity to CDDP in cancer cells both in vitro and in vivo. Our results suggest that the combination of CDDP and Rad51 siRNA will be an effective anti‐cancer protocol. Copyright © 2005 John Wiley & Sons, Ltd.</abstract><qualityIndicators><score>10</score><pdfWordCount>5467</pdfWordCount><pdfCharCount>33411</pdfCharCount><pdfVersion>1.3</pdfVersion><pdfPageCount>9</pdfPageCount><pdfPageSize>595 x 859 pts</pdfPageSize><pdfWordsPerPage>607</pdfWordsPerPage><pdfText>true</pdfText><refBibsNative>true</refBibsNative><abstractWordCount>324</abstractWordCount><abstractCharCount>2141</abstractCharCount><keywordCount>6</keywordCount></qualityIndicators><title>Rad51 siRNA delivered by HVJ envelope vector enhances the anti‐cancer effect of cisplatin</title><pmid><json:string>15756713</json:string></pmid><genre><json:string>article</json:string></genre><host><title>The Journal of Gene Medicine</title><language><json:string>unknown</json:string></language><doi><json:string>10.1002/(ISSN)1521-2254</json:string></doi><issn><json:string>1099-498X</json:string></issn><eissn><json:string>1521-2254</json:string></eissn><publisherId><json:string>JGM</json:string></publisherId><volume>7</volume><issue>8</issue><pages><first>1044</first><last>1052</last><total>9</total></pages><genre><json:string>journal</json:string></genre><subject><json:item><value>Research Article</value></json:item><json:item><value>Research Articles</value></json:item></subject></host><namedEntities><unitex><date><json:string>2005</json:string></date><geogName></geogName><orgName><json:string>Osaka University</json:string><json:string>Division of Gene Therapy Science</json:string><json:string>Animal Committee of Osaka University</json:string><json:string>Lafayette, CO</json:string><json:string>Charles River Japan, Yokohama, Japan</json:string><json:string>Sons, Ltd.</json:string><json:string>Japan, Sendai</json:string><json:string>Coulter Corporation, Miami</json:string><json:string>Ministry of Education, Culture, Sports, Science and Technology of Japan</json:string><json:string>Sons, Ltd</json:string></orgName><orgName_funder></orgName_funder><orgName_provider></orgName_provider><persName><json:string>Y. 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Vector</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>John Wiley & Sons, Ltd.</publisher><pubPlace>Chichester, UK</pubPlace><availability><licence>Copyright © 2005 John Wiley & Sons, Ltd.</licence></availability><date type="published" when="2005-08"></date></publicationStmt><notesStmt><note type="content-type" subtype="article" source="article" scheme="https://content-type.data.istex.fr/ark:/67375/XTP-6N5SZHKN-D">article</note><note type="publication-type" subtype="journal" scheme="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">journal</note></notesStmt><sourceDesc><biblStruct type="article"><analytic><title level="a" type="main">Rad51 siRNA delivered by HVJ envelope vector enhances the anti‐cancer effect of cisplatin</title><title level="a" type="short" xml:lang="en">Rad51 siRNA Delivered by HVJ Envelope Vector</title><author xml:id="author-0000"><persName><forename type="first">Makoto</forename><surname>Ito</surname></persName><affiliation><orgName type="division">Division of Gene Therapy Science</orgName><orgName type="department">Graduate School of Medicine</orgName><orgName type="institution">Osaka University</orgName><address><addrLine>2‐2 Yamada‐oka</addrLine><addrLine>Suita, Osaka 565 ‐0871, Japan</addrLine><country key="JP" xml:lang="en">JAPAN</country></address></affiliation></author><author xml:id="author-0001"><persName><forename type="first">Seiji</forename><surname>Yamamoto</surname></persName><affiliation><orgName type="division">Division of Gene Therapy Science</orgName><orgName type="department">Graduate School of Medicine</orgName><orgName type="institution">Osaka University</orgName><address><addrLine>2‐2 Yamada‐oka</addrLine><addrLine>Suita, Osaka 565 ‐0871, Japan</addrLine><country key="JP" xml:lang="en">JAPAN</country></address></affiliation></author><author xml:id="author-0002"><persName><forename type="first">Keisuke</forename><surname>Nimura</surname></persName><affiliation><orgName type="division">Division of Gene Therapy Science</orgName><orgName type="department">Graduate School of Medicine</orgName><orgName type="institution">Osaka University</orgName><address><addrLine>2‐2 Yamada‐oka</addrLine><addrLine>Suita, Osaka 565 ‐0871, Japan</addrLine><country key="JP" xml:lang="en">JAPAN</country></address></affiliation></author><author xml:id="author-0003"><persName><forename type="first">Kazuya</forename><surname>Hiraoka</surname></persName><affiliation><orgName type="division">Division of Gene Therapy Science</orgName><orgName type="department">Graduate School of Medicine</orgName><orgName type="institution">Osaka University</orgName><address><addrLine>2‐2 Yamada‐oka</addrLine><addrLine>Suita, Osaka 565 ‐0871, Japan</addrLine><country key="JP" xml:lang="en">JAPAN</country></address></affiliation></author><author xml:id="author-0004"><persName><forename type="first">Katsuto</forename><surname>Tamai</surname></persName><affiliation><orgName type="division">Division of Gene Therapy Science</orgName><orgName type="department">Graduate School of Medicine</orgName><orgName type="institution">Osaka University</orgName><address><addrLine>2‐2 Yamada‐oka</addrLine><addrLine>Suita, Osaka 565 ‐0871, Japan</addrLine><country key="JP" xml:lang="en">JAPAN</country></address></affiliation></author><author xml:id="author-0005" role="corresp"><persName><forename type="first">Yasufumi</forename><surname>Kaneda</surname></persName><email>kaneday@gts.med.osaka‐u.ac.jp</email><affiliation><orgName type="division">Division of Gene Therapy Science</orgName><orgName type="department">Graduate School of Medicine</orgName><orgName type="institution">Osaka University</orgName><address><addrLine>2‐2 Yamada‐oka</addrLine><addrLine>Suita, Osaka 565 ‐0871, Japan</addrLine><country key="JP" xml:lang="en">JAPAN</country></address></affiliation></author><idno 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when="2005-08"></date></imprint></monogr></biblStruct></sourceDesc></fileDesc><encodingDesc><schemaRef type="ODD" url="https://xml-schema.delivery.istex.fr/tei-istex.odd"></schemaRef><appInfo><application ident="pub2tei" version="1.0.10" when="2019-12-20"><label>pub2TEI-ISTEX</label><desc>A set of style sheets for converting XML documents encoded in various scientific publisher formats into a common TEI format.
<ref target="http://www.tei-c.org/">We use TEI</ref></desc></application></appInfo></encodingDesc><profileDesc><abstract xml:lang="en" style="main"><head>Abstract</head><head>Background</head><p>Every cancer therapy appears to be transiently effective for cancer regression, but cancers gradually transform to be resistant to the therapy. Cancers also develop machineries to resist chemotherapy. Short interfering RNA (siRNA) has been evaluated as an attractive and effective tool for suppressing a target protein by specifically digesting its mRNA. Suppression of the machineries using siRNA may enhance the sensitivity to chemotherapy in cancers when combined with an effective delivery system.</p><head>Methods</head><p>To enhance the anti‐cancer effect of chemotherapy, we transferred siRNA against Rad51 into various human cancer cells using the HVJ (hemagglutinating virus of Japan, Sendai virus) envelope vector in the presence or absence of cis‐diamminedichloroplatinum(II) (CDDP, cisplatin). The inhibition of cell growth was assessed by a modified MTT assay, counting cell number, or fluorescence‐activated cell sorting (FACS) analysis after Annexin V labeling. The synthetic Rad51 siRNA was also introduced into subcutaneous tumor masses of HeLa cells in SCID mice with or without intraperitoneal injection of CDDP, and tumor growth was monitored.</p><head>Results</head><p>When synthetic Rad51 siRNA was delivered into HeLa cells using the HVJ envelope vector, no Rad51 transcripts were detected on day 2, and Rad51 protein completely disappeared for 4 days after siRNA transfer. When HeLa cells were incubated with 0.02 µg/ml CDDP for 3 h after siRNA transfer, the number of colonies decreased to approximately 10% of that with scrambled siRNA. The sensitivity to CDDP was enhanced in various human cancer cells, but not in normal human fibroblasts. When Rad51 siRNA was delivered into tumors using the HVJ envelope vector, the Rad51 transcript level was reduced to approximately 25%. Rad51 siRNA combined with CDDP significantly inhibited tumor growth when compared to siRNA or CDDP alone.</p><head>Conclusions</head><p>Rad51 siRNA could enhance the sensitivity to CDDP in cancer cells both <hi rend="italic">in vitro</hi> and <hi rend="italic">in vivo</hi>. Our results suggest that the combination of CDDP and Rad51 siRNA will be an effective anti‐cancer protocol. Copyright © 2005 John Wiley & Sons, Ltd.</p></abstract><textClass><keywords xml:lang="en"><term xml:id="kwd1">chemotherapy</term><term xml:id="kwd2">siRNA</term><term xml:id="kwd3">Rad51</term><term xml:id="kwd4">non‐viral vector</term><term xml:id="kwd5">drug delivery</term><term xml:id="kwd6">cancer therapy</term></keywords><keywords rend="articleCategory"><term>Research Article</term></keywords><keywords rend="tocHeading1"><term>Research Articles</term></keywords></textClass><langUsage><language ident="en"></language></langUsage></profileDesc><revisionDesc><change when="2019-12-20" who="#istex" xml:id="pub2tei">formatting</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/ark:/67375/WNG-GLHFLM13-6/fulltext.txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Wiley, elements deleted: body"><istex:xmlDeclaration>version="1.0" encoding="UTF-8" standalone="yes"</istex:xmlDeclaration><istex:document><component version="2.0" type="serialArticle" xml:lang="en"><header><publicationMeta level="product"><publisherInfo><publisherName>John Wiley & Sons, Ltd.</publisherName><publisherLoc>Chichester, UK</publisherLoc></publisherInfo><doi registered="yes">10.1002/(ISSN)1521-2254</doi><issn type="print">1099-498X</issn><issn type="electronic">1521-2254</issn><idGroup><id type="product" value="JGM"></id></idGroup><titleGroup><title type="main" xml:lang="en" sort="JOURNAL OF GENE MEDICINE, THE">The Journal of Gene Medicine</title><title type="subtitle">A cross‐disciplinary journal for research on the science of gene transfer and its clinical applications</title><title type="short">J. Gene Med.</title></titleGroup></publicationMeta><publicationMeta level="part" position="80"><doi origin="wiley" registered="yes">10.1002/jgm.v7:8</doi><numberingGroup><numbering type="journalVolume" number="7">7</numbering><numbering type="journalIssue">8</numbering></numberingGroup><coverDate startDate="2005-08">August 2005</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="6" status="forIssue"><doi origin="wiley" registered="yes">10.1002/jgm.753</doi><idGroup><id type="unit" value="JGM753"></id></idGroup><countGroup><count type="pageTotal" number="9"></count></countGroup><titleGroup><title type="articleCategory">Research Article</title><title type="tocHeading1">Research Articles</title></titleGroup><copyright ownership="publisher">Copyright © 2005 John Wiley & Sons, Ltd.</copyright><eventGroup><event type="manuscriptReceived" date="2004-09-27"></event><event type="manuscriptRevised" date="2004-12-04"></event><event type="manuscriptAccepted" date="2005-01-04"></event><event type="publishedOnlineEarlyUnpaginated" date="2005-03-08"></event><event type="firstOnline" date="2005-03-08"></event><event type="publishedOnlineFinalForm" date="2005-08-01"></event><event type="xmlConverted" agent="Converter:JWSART34_TO_WML3G version:2.3.2 mode:FullText source:FullText result:FullText" date="2010-03-04"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:3.8.8" date="2014-01-30"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.1.7 mode:FullText,remove_FC" date="2014-11-04"></event></eventGroup><numberingGroup><numbering type="pageFirst">1044</numbering><numbering type="pageLast">1052</numbering></numberingGroup><correspondenceTo>Division of Gene Therapy Science, Graduate School of Medicine, Osaka University, 2‐2 Yamada‐oka, Suita, Osaka 565‐0871, Japan.</correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:JGM.JGM753.pdf"></link></linkGroup></publicationMeta><contentMeta><countGroup><count type="figureTotal" number="8"></count><count type="tableTotal" number="0"></count><count type="referenceTotal" number="43"></count></countGroup><titleGroup><title type="main" xml:lang="en">Rad51 siRNA delivered by HVJ envelope vector enhances the anti‐cancer effect of cisplatin</title><title type="short" xml:lang="en">Rad51 siRNA Delivered by HVJ Envelope Vector</title></titleGroup><creators><creator xml:id="au1" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Makoto</givenNames><familyName>Ito</familyName></personName></creator><creator xml:id="au2" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Seiji</givenNames><familyName>Yamamoto</familyName></personName></creator><creator xml:id="au3" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Keisuke</givenNames><familyName>Nimura</familyName></personName></creator><creator xml:id="au4" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Kazuya</givenNames><familyName>Hiraoka</familyName></personName></creator><creator xml:id="au5" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Katsuto</givenNames><familyName>Tamai</familyName></personName></creator><creator xml:id="au6" creatorRole="author" affiliationRef="#af1" corresponding="yes"><personName><givenNames>Yasufumi</givenNames><familyName>Kaneda</familyName></personName><contactDetails><email normalForm="kaneday@gts.med.osaka-u.ac.jp">kaneday@gts.med.osaka‐u.ac.jp</email></contactDetails></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="JP" type="organization"><unparsedAffiliation>Division of Gene Therapy Science, Graduate School of Medicine, Osaka University, 2‐2 Yamada‐oka, Suita, Osaka 565 ‐0871, Japan</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1">chemotherapy</keyword><keyword xml:id="kwd2">siRNA</keyword><keyword xml:id="kwd3">Rad51</keyword><keyword xml:id="kwd4">non‐viral vector</keyword><keyword xml:id="kwd5">drug delivery</keyword><keyword xml:id="kwd6">cancer therapy</keyword></keywordGroup><fundingInfo><fundingAgency>Ministry of Education, Culture, Sports, Science and Technology of Japan</fundingAgency><fundingNumber>15300163</fundingNumber></fundingInfo><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><section xml:id="abs1-1"><title type="main">Background</title><p>Every cancer therapy appears to be transiently effective for cancer regression, but cancers gradually transform to be resistant to the therapy. Cancers also develop machineries to resist chemotherapy. Short interfering RNA (siRNA) has been evaluated as an attractive and effective tool for suppressing a target protein by specifically digesting its mRNA. Suppression of the machineries using siRNA may enhance the sensitivity to chemotherapy in cancers when combined with an effective delivery system.</p></section><section xml:id="abs1-2"><title type="main">Methods</title><p>To enhance the anti‐cancer effect of chemotherapy, we transferred siRNA against Rad51 into various human cancer cells using the HVJ (hemagglutinating virus of Japan, Sendai virus) envelope vector in the presence or absence of cis‐diamminedichloroplatinum(II) (CDDP, cisplatin). The inhibition of cell growth was assessed by a modified MTT assay, counting cell number, or fluorescence‐activated cell sorting (FACS) analysis after Annexin V labeling. The synthetic Rad51 siRNA was also introduced into subcutaneous tumor masses of HeLa cells in SCID mice with or without intraperitoneal injection of CDDP, and tumor growth was monitored.</p></section><section xml:id="abs1-3"><title type="main">Results</title><p>When synthetic Rad51 siRNA was delivered into HeLa cells using the HVJ envelope vector, no Rad51 transcripts were detected on day 2, and Rad51 protein completely disappeared for 4 days after siRNA transfer. When HeLa cells were incubated with 0.02 µg/ml CDDP for 3 h after siRNA transfer, the number of colonies decreased to approximately 10% of that with scrambled siRNA. The sensitivity to CDDP was enhanced in various human cancer cells, but not in normal human fibroblasts. When Rad51 siRNA was delivered into tumors using the HVJ envelope vector, the Rad51 transcript level was reduced to approximately 25%. Rad51 siRNA combined with CDDP significantly inhibited tumor growth when compared to siRNA or CDDP alone.</p></section><section xml:id="abs1-4"><title type="main">Conclusions</title><p>Rad51 siRNA could enhance the sensitivity to CDDP in cancer cells both <i>in vitro</i> and <i>in vivo</i>. Our results suggest that the combination of CDDP and Rad51 siRNA will be an effective anti‐cancer protocol. Copyright © 2005 John Wiley & Sons, Ltd.</p></section></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Rad51 siRNA delivered by HVJ envelope vector enhances the anti‐cancer effect of cisplatin</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Rad51 siRNA Delivered by HVJ Envelope Vector</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Rad51 siRNA delivered by HVJ envelope vector enhances the anti‐cancer effect of cisplatin</title></titleInfo><name type="personal"><namePart type="given">Makoto</namePart><namePart type="family">Ito</namePart><affiliation>Division of Gene Therapy Science, Graduate School of Medicine, Osaka University, 2‐2 Yamada‐oka, Suita, Osaka 565 ‐0871, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Seiji</namePart><namePart type="family">Yamamoto</namePart><affiliation>Division of Gene Therapy Science, Graduate School of Medicine, Osaka University, 2‐2 Yamada‐oka, Suita, Osaka 565 ‐0871, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Keisuke</namePart><namePart type="family">Nimura</namePart><affiliation>Division of Gene Therapy Science, Graduate School of Medicine, Osaka University, 2‐2 Yamada‐oka, Suita, Osaka 565 ‐0871, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Kazuya</namePart><namePart type="family">Hiraoka</namePart><affiliation>Division of Gene Therapy Science, Graduate School of Medicine, Osaka University, 2‐2 Yamada‐oka, Suita, Osaka 565 ‐0871, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Katsuto</namePart><namePart type="family">Tamai</namePart><affiliation>Division of Gene Therapy Science, Graduate School of Medicine, Osaka University, 2‐2 Yamada‐oka, Suita, Osaka 565 ‐0871, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Yasufumi</namePart><namePart type="family">Kaneda</namePart><affiliation>Division of Gene Therapy Science, Graduate School of Medicine, Osaka University, 2‐2 Yamada‐oka, Suita, Osaka 565 ‐0871, Japan</affiliation><affiliation>E-mail: kaneday@gts.med.osaka‐u.ac.jp</affiliation><affiliation>Correspondence address: Division of Gene Therapy Science, Graduate School of Medicine, Osaka University, 2‐2 Yamada‐oka, Suita, Osaka 565‐0871, Japan.</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article" authority="ISTEX" authorityURI="https://content-type.data.istex.fr" valueURI="https://content-type.data.istex.fr/ark:/67375/XTP-6N5SZHKN-D">article</genre><originInfo><publisher>John Wiley & Sons, Ltd.</publisher><place><placeTerm type="text">Chichester, UK</placeTerm></place><dateIssued encoding="w3cdtf">2005-08</dateIssued><dateCaptured encoding="w3cdtf">2004-09-27</dateCaptured><dateValid encoding="w3cdtf">2005-01-04</dateValid><copyrightDate encoding="w3cdtf">2005</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><extent unit="figures">8</extent><extent unit="tables">0</extent><extent unit="references">43</extent></physicalDescription><abstract lang="en">Background: Every cancer therapy appears to be transiently effective for cancer regression, but cancers gradually transform to be resistant to the therapy. Cancers also develop machineries to resist chemotherapy. Short interfering RNA (siRNA) has been evaluated as an attractive and effective tool for suppressing a target protein by specifically digesting its mRNA. Suppression of the machineries using siRNA may enhance the sensitivity to chemotherapy in cancers when combined with an effective delivery system. Methods: To enhance the anti‐cancer effect of chemotherapy, we transferred siRNA against Rad51 into various human cancer cells using the HVJ (hemagglutinating virus of Japan, Sendai virus) envelope vector in the presence or absence of cis‐diamminedichloroplatinum(II) (CDDP, cisplatin). The inhibition of cell growth was assessed by a modified MTT assay, counting cell number, or fluorescence‐activated cell sorting (FACS) analysis after Annexin V labeling. The synthetic Rad51 siRNA was also introduced into subcutaneous tumor masses of HeLa cells in SCID mice with or without intraperitoneal injection of CDDP, and tumor growth was monitored. Results: When synthetic Rad51 siRNA was delivered into HeLa cells using the HVJ envelope vector, no Rad51 transcripts were detected on day 2, and Rad51 protein completely disappeared for 4 days after siRNA transfer. When HeLa cells were incubated with 0.02 µg/ml CDDP for 3 h after siRNA transfer, the number of colonies decreased to approximately 10% of that with scrambled siRNA. The sensitivity to CDDP was enhanced in various human cancer cells, but not in normal human fibroblasts. When Rad51 siRNA was delivered into tumors using the HVJ envelope vector, the Rad51 transcript level was reduced to approximately 25%. Rad51 siRNA combined with CDDP significantly inhibited tumor growth when compared to siRNA or CDDP alone. Conclusions: Rad51 siRNA could enhance the sensitivity to CDDP in cancer cells both in vitro and in vivo. Our results suggest that the combination of CDDP and Rad51 siRNA will be an effective anti‐cancer protocol. Copyright © 2005 John Wiley & Sons, Ltd.</abstract><note type="funding">Ministry of Education, Culture, Sports, Science and Technology of Japan - No. 15300163; </note><subject lang="en"><genre>keywords</genre><topic>chemotherapy</topic><topic>siRNA</topic><topic>Rad51</topic><topic>non‐viral vector</topic><topic>drug delivery</topic><topic>cancer therapy</topic></subject><relatedItem type="host"><titleInfo><title>The Journal of Gene Medicine</title><subTitle>A cross‐disciplinary journal for research on the science of gene transfer and its clinical applications</subTitle></titleInfo><titleInfo type="abbreviated"><title>J. 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