RNA Interference Using c-Myc-Conjugated Nanoparticles Suppresses Breast and Colorectal Cancer Models.
Identifieur interne : 002E11 ( PubMed/Corpus ); précédent : 002E10; suivant : 002E12RNA Interference Using c-Myc-Conjugated Nanoparticles Suppresses Breast and Colorectal Cancer Models.
Auteurs : Naveen K. Tangudu ; Vinod K. Verma ; Tristan D. Clemons ; Syed S. Beevi ; Trevor Hay ; Ganesh Mahidhara ; Meera Raja ; Rekha A. Nair ; Liza E. Alexander ; Anant B. Patel ; Jedy Jose ; Nicole M. Smith ; Bogdan Zdyrko ; Anne Bourdoncle ; Igor Luzinov ; K Swaminathan Iyer ; Alan R. Clarke ; Lekha Dinesh KumarSource :
- Molecular cancer therapeutics [ 1538-8514 ] ; 2015.
English descriptors
- KwdEn :
- Animals, Breast Neoplasms (genetics), Breast Neoplasms (therapy), Cell Line, Tumor, Colorectal Neoplasms (genetics), Colorectal Neoplasms (therapy), Female, Gene Silencing, HEK293 Cells, Humans, Jurkat Cells, MCF-7 Cells, Mice, NIH 3T3 Cells, Nanoconjugates, Neoplasm Transplantation, Oligonucleotides, Antisense (administration & dosage), Polypropylenes (chemistry), Proto-Oncogene Proteins c-myc (antagonists & inhibitors), RNA Interference, RNAi Therapeutics (methods).
- MESH :
- chemical , administration & dosage : Oligonucleotides, Antisense.
- chemical , antagonists & inhibitors : Proto-Oncogene Proteins c-myc.
- chemical , chemistry : Polypropylenes.
- chemical : Nanoconjugates.
- genetics : Breast Neoplasms, Colorectal Neoplasms.
- methods : RNAi Therapeutics.
- therapy : Breast Neoplasms, Colorectal Neoplasms.
- Animals, Cell Line, Tumor, Female, Gene Silencing, HEK293 Cells, Humans, Jurkat Cells, MCF-7 Cells, Mice, NIH 3T3 Cells, Neoplasm Transplantation, RNA Interference.
Abstract
In this article, we report the development and preclinical validation of combinatorial therapy for treatment of cancers using RNA interference (RNAi). RNAi technology is an attractive approach to silence genes responsible for disease onset and progression. Currently, the critical challenge facing the clinical success of RNAi technology is in the difficulty of delivery of RNAi inducers, due to low transfection efficiency, difficulties of integration into host DNA and unstable expression. Using the macromolecule polyglycidal methacrylate (PGMA) as a platform to graft multiple polyethyleneimine (PEI) chains, we demonstrate effective delivery of small oligos (anti-miRs and mimics) and larger DNAs (encoding shRNAs) in a wide variety of cancer cell lines by successful silencing/activation of their respective target genes. Furthermore, the effectiveness of this therapy was validated for in vivo tumor suppression using two transgenic mouse models; first, tumor growth arrest and increased animal survival was seen in mice bearing Brca2/p53-mutant mammary tumors following daily intratumoral treatment with nanoparticles conjugated to c-Myc shRNA. Second, oral delivery of the conjugate to an Apc-deficient crypt progenitor colon cancer model increased animal survival and returned intestinal tissue to a non-wnt-deregulated state. This study demonstrates, through careful design of nonviral nanoparticles and appropriate selection of therapeutic gene targets, that RNAi technology can be made an affordable and amenable therapy for cancer.
DOI: 10.1158/1535-7163.MCT-14-0970
PubMed: 25695957
Links to Exploration step
pubmed:25695957Le document en format XML
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<sourceDesc><biblStruct><analytic><title xml:lang="en">RNA Interference Using c-Myc-Conjugated Nanoparticles Suppresses Breast and Colorectal Cancer Models.</title>
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<author><name sortKey="Hay, Trevor" sort="Hay, Trevor" uniqKey="Hay T" first="Trevor" last="Hay">Trevor Hay</name>
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<author><name sortKey="Mahidhara, Ganesh" sort="Mahidhara, Ganesh" uniqKey="Mahidhara G" first="Ganesh" last="Mahidhara">Ganesh Mahidhara</name>
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<term>Cell Line, Tumor</term>
<term>Colorectal Neoplasms (genetics)</term>
<term>Colorectal Neoplasms (therapy)</term>
<term>Female</term>
<term>Gene Silencing</term>
<term>HEK293 Cells</term>
<term>Humans</term>
<term>Jurkat Cells</term>
<term>MCF-7 Cells</term>
<term>Mice</term>
<term>NIH 3T3 Cells</term>
<term>Nanoconjugates</term>
<term>Neoplasm Transplantation</term>
<term>Oligonucleotides, Antisense (administration & dosage)</term>
<term>Polypropylenes (chemistry)</term>
<term>Proto-Oncogene Proteins c-myc (antagonists & inhibitors)</term>
<term>RNA Interference</term>
<term>RNAi Therapeutics (methods)</term>
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<term>Colorectal Neoplasms</term>
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<term>Colorectal Neoplasms</term>
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<term>Gene Silencing</term>
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<term>Humans</term>
<term>Jurkat Cells</term>
<term>MCF-7 Cells</term>
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<front><div type="abstract" xml:lang="en">In this article, we report the development and preclinical validation of combinatorial therapy for treatment of cancers using RNA interference (RNAi). RNAi technology is an attractive approach to silence genes responsible for disease onset and progression. Currently, the critical challenge facing the clinical success of RNAi technology is in the difficulty of delivery of RNAi inducers, due to low transfection efficiency, difficulties of integration into host DNA and unstable expression. Using the macromolecule polyglycidal methacrylate (PGMA) as a platform to graft multiple polyethyleneimine (PEI) chains, we demonstrate effective delivery of small oligos (anti-miRs and mimics) and larger DNAs (encoding shRNAs) in a wide variety of cancer cell lines by successful silencing/activation of their respective target genes. Furthermore, the effectiveness of this therapy was validated for in vivo tumor suppression using two transgenic mouse models; first, tumor growth arrest and increased animal survival was seen in mice bearing Brca2/p53-mutant mammary tumors following daily intratumoral treatment with nanoparticles conjugated to c-Myc shRNA. Second, oral delivery of the conjugate to an Apc-deficient crypt progenitor colon cancer model increased animal survival and returned intestinal tissue to a non-wnt-deregulated state. This study demonstrates, through careful design of nonviral nanoparticles and appropriate selection of therapeutic gene targets, that RNAi technology can be made an affordable and amenable therapy for cancer.</div>
</front>
</TEI>
<pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">25695957</PMID>
<DateCreated><Year>2015</Year>
<Month>05</Month>
<Day>07</Day>
</DateCreated>
<DateCompleted><Year>2016</Year>
<Month>02</Month>
<Day>01</Day>
</DateCompleted>
<DateRevised><Year>2015</Year>
<Month>05</Month>
<Day>07</Day>
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<Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1538-8514</ISSN>
<JournalIssue CitedMedium="Internet"><Volume>14</Volume>
<Issue>5</Issue>
<PubDate><Year>2015</Year>
<Month>May</Month>
</PubDate>
</JournalIssue>
<Title>Molecular cancer therapeutics</Title>
<ISOAbbreviation>Mol. Cancer Ther.</ISOAbbreviation>
</Journal>
<ArticleTitle>RNA Interference Using c-Myc-Conjugated Nanoparticles Suppresses Breast and Colorectal Cancer Models.</ArticleTitle>
<Pagination><MedlinePgn>1259-69</MedlinePgn>
</Pagination>
<ELocationID EIdType="doi" ValidYN="Y">10.1158/1535-7163.MCT-14-0970</ELocationID>
<Abstract><AbstractText>In this article, we report the development and preclinical validation of combinatorial therapy for treatment of cancers using RNA interference (RNAi). RNAi technology is an attractive approach to silence genes responsible for disease onset and progression. Currently, the critical challenge facing the clinical success of RNAi technology is in the difficulty of delivery of RNAi inducers, due to low transfection efficiency, difficulties of integration into host DNA and unstable expression. Using the macromolecule polyglycidal methacrylate (PGMA) as a platform to graft multiple polyethyleneimine (PEI) chains, we demonstrate effective delivery of small oligos (anti-miRs and mimics) and larger DNAs (encoding shRNAs) in a wide variety of cancer cell lines by successful silencing/activation of their respective target genes. Furthermore, the effectiveness of this therapy was validated for in vivo tumor suppression using two transgenic mouse models; first, tumor growth arrest and increased animal survival was seen in mice bearing Brca2/p53-mutant mammary tumors following daily intratumoral treatment with nanoparticles conjugated to c-Myc shRNA. Second, oral delivery of the conjugate to an Apc-deficient crypt progenitor colon cancer model increased animal survival and returned intestinal tissue to a non-wnt-deregulated state. This study demonstrates, through careful design of nonviral nanoparticles and appropriate selection of therapeutic gene targets, that RNAi technology can be made an affordable and amenable therapy for cancer.</AbstractText>
<CopyrightInformation>©2015 American Association for Cancer Research.</CopyrightInformation>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Tangudu</LastName>
<ForeName>Naveen K</ForeName>
<Initials>NK</Initials>
<AffiliationInfo><Affiliation>Cancer Biology, Centre for Cellular and Molecular Biology, Council of Scientific and Industrial Research, Hyderabad, India.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Verma</LastName>
<ForeName>Vinod K</ForeName>
<Initials>VK</Initials>
<AffiliationInfo><Affiliation>Cancer Biology, Centre for Cellular and Molecular Biology, Council of Scientific and Industrial Research, Hyderabad, India.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Clemons</LastName>
<ForeName>Tristan D</ForeName>
<Initials>TD</Initials>
<AffiliationInfo><Affiliation>School of Chemistry and Biochemistry, The University of Western Australia, Crawley, Australia.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Beevi</LastName>
<ForeName>Syed S</ForeName>
<Initials>SS</Initials>
<AffiliationInfo><Affiliation>Cancer Biology, Centre for Cellular and Molecular Biology, Council of Scientific and Industrial Research, Hyderabad, India.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Hay</LastName>
<ForeName>Trevor</ForeName>
<Initials>T</Initials>
<AffiliationInfo><Affiliation>European Cancer Stem Cell Research Institute, Cardiff University, Cathays, Cardiff, United Kingdom.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Mahidhara</LastName>
<ForeName>Ganesh</ForeName>
<Initials>G</Initials>
<AffiliationInfo><Affiliation>Cancer Biology, Centre for Cellular and Molecular Biology, Council of Scientific and Industrial Research, Hyderabad, India.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Raja</LastName>
<ForeName>Meera</ForeName>
<Initials>M</Initials>
<AffiliationInfo><Affiliation>European Cancer Stem Cell Research Institute, Cardiff University, Cathays, Cardiff, United Kingdom.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Nair</LastName>
<ForeName>Rekha A</ForeName>
<Initials>RA</Initials>
<AffiliationInfo><Affiliation>Department of Pathology, Regional Cancer Centre, Trivandrum, India.</Affiliation>
</AffiliationInfo>
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<Author ValidYN="Y"><LastName>Alexander</LastName>
<ForeName>Liza E</ForeName>
<Initials>LE</Initials>
<AffiliationInfo><Affiliation>Department of Pathology, Regional Cancer Centre, Trivandrum, India.</Affiliation>
</AffiliationInfo>
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<Author ValidYN="Y"><LastName>Patel</LastName>
<ForeName>Anant B</ForeName>
<Initials>AB</Initials>
<AffiliationInfo><Affiliation>Cancer Biology, Centre for Cellular and Molecular Biology, Council of Scientific and Industrial Research, Hyderabad, India.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Jose</LastName>
<ForeName>Jedy</ForeName>
<Initials>J</Initials>
<AffiliationInfo><Affiliation>Cancer Biology, Centre for Cellular and Molecular Biology, Council of Scientific and Industrial Research, Hyderabad, India.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Smith</LastName>
<ForeName>Nicole M</ForeName>
<Initials>NM</Initials>
<AffiliationInfo><Affiliation>Univ de Bordeaux, INSERM U869, IECB, ARNA Laboratory, Pessac, France.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Zdyrko</LastName>
<ForeName>Bogdan</ForeName>
<Initials>B</Initials>
<AffiliationInfo><Affiliation>School of Materials Science and Engineering, Clemson University, Clemson, South Carolina.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Bourdoncle</LastName>
<ForeName>Anne</ForeName>
<Initials>A</Initials>
<AffiliationInfo><Affiliation>Univ de Bordeaux, INSERM U869, IECB, ARNA Laboratory, Pessac, France.</Affiliation>
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