pcDNA3.1(−)-mediated ribozyme targeting of HER-2 suppresses breast cancer tumor growth
The HER-2 proto-oncogene (also called c-erbB-2/neu) encodes the protein, p185, which is closely related to the growth and metastasis of adenocarcinoma, and is overexpressed in 25–30% of human breast cancers. In this study, we attempt to reverse the malignant phenotype of the breast cancer cell line,...
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| Veröffentlicht in: | Molecular biology reports 2010-03, Vol.37 (3), p.1597-1604 |
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| creator | He, Pei Zhu, Dan Hu, Jun-Jian Peng, Ju Chen, Lian-Sheng Lu, Guang-Xiu |
| description | The
HER-2
proto-oncogene (also called c-erbB-2/neu) encodes the protein, p185, which is closely related to the growth and metastasis of adenocarcinoma, and is overexpressed in 25–30% of human breast cancers. In this study, we attempt to reverse the malignant phenotype of the breast cancer cell line, MCF-7, using a
HER-2
-specific hammerhead ribozyme. Two anti-
HER-2
hammerhead ribozymes, RZ1 and RZ2, were synthesized, inserted separately into the nonviral eukaryotic expression vector, pcDNA3.1(−), and transfected into MCF-7 cells. Analyses showed that the
HER-2
mRNA and p185, as well as oncogene
k-ras
were down-regulated remarkably in the ribozyme-transfected cells, while the onco-suppressor gene,
p53
, was up-regulated. Furthermore, the tumorigenicity of the RZ1-stably transfected MCF-7 cells was decreased dramatically in nude mice. These results demonstrate that the use of anti-
HER-2
ribozymes may be a beneficial strategy for gene therapy of breast cancer. |
| doi_str_mv | 10.1007/s11033-009-9569-4 |
| format | Article |
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HER-2
proto-oncogene (also called c-erbB-2/neu) encodes the protein, p185, which is closely related to the growth and metastasis of adenocarcinoma, and is overexpressed in 25–30% of human breast cancers. In this study, we attempt to reverse the malignant phenotype of the breast cancer cell line, MCF-7, using a
HER-2
-specific hammerhead ribozyme. Two anti-
HER-2
hammerhead ribozymes, RZ1 and RZ2, were synthesized, inserted separately into the nonviral eukaryotic expression vector, pcDNA3.1(−), and transfected into MCF-7 cells. Analyses showed that the
HER-2
mRNA and p185, as well as oncogene
k-ras
were down-regulated remarkably in the ribozyme-transfected cells, while the onco-suppressor gene,
p53
, was up-regulated. Furthermore, the tumorigenicity of the RZ1-stably transfected MCF-7 cells was decreased dramatically in nude mice. These results demonstrate that the use of anti-
HER-2
ribozymes may be a beneficial strategy for gene therapy of breast cancer.</description><identifier>ISSN: 0301-4851</identifier><identifier>EISSN: 1573-4978</identifier><identifier>DOI: 10.1007/s11033-009-9569-4</identifier><identifier>PMID: 19444644</identifier><language>eng</language><publisher>Dordrecht: Springer Netherlands</publisher><subject>Adenocarcinoma - therapy ; Animal Anatomy ; Animal Biochemistry ; Animals ; Biomedical and Life Sciences ; Blotting, Western ; Breast cancer ; Breast Neoplasms - therapy ; Cell Line, Tumor ; DNA Primers - genetics ; Female ; Flow Cytometry ; Gene expression ; Gene Expression Regulation, Neoplastic - genetics ; Gene Targeting - methods ; Gene therapy ; Genetic Therapy - methods ; Genetic Vectors - genetics ; Genotype & phenotype ; Histology ; Humans ; Life Sciences ; Mice ; Mice, Nude ; Morphology ; Oncology ; Proteins ; Receptor, ErbB-2 - genetics ; Receptor, ErbB-2 - metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; RNA, Catalytic - genetics ; RNA, Catalytic - pharmacology ; Transfection</subject><ispartof>Molecular biology reports, 2010-03, Vol.37 (3), p.1597-1604</ispartof><rights>Springer Science+Business Media B.V. 2009</rights><rights>Springer Science+Business Media B.V. 2010</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c402t-9b68cc8e43b93228782b68604775bc485229d9e36f6646c6a62dc52aad05b3bb3</citedby><cites>FETCH-LOGICAL-c402t-9b68cc8e43b93228782b68604775bc485229d9e36f6646c6a62dc52aad05b3bb3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s11033-009-9569-4$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s11033-009-9569-4$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27903,27904,41467,42536,51297</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19444644$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>He, Pei</creatorcontrib><creatorcontrib>Zhu, Dan</creatorcontrib><creatorcontrib>Hu, Jun-Jian</creatorcontrib><creatorcontrib>Peng, Ju</creatorcontrib><creatorcontrib>Chen, Lian-Sheng</creatorcontrib><creatorcontrib>Lu, Guang-Xiu</creatorcontrib><title>pcDNA3.1(−)-mediated ribozyme targeting of HER-2 suppresses breast cancer tumor growth</title><title>Molecular biology reports</title><addtitle>Mol Biol Rep</addtitle><addtitle>Mol Biol Rep</addtitle><description>The
HER-2
proto-oncogene (also called c-erbB-2/neu) encodes the protein, p185, which is closely related to the growth and metastasis of adenocarcinoma, and is overexpressed in 25–30% of human breast cancers. In this study, we attempt to reverse the malignant phenotype of the breast cancer cell line, MCF-7, using a
HER-2
-specific hammerhead ribozyme. Two anti-
HER-2
hammerhead ribozymes, RZ1 and RZ2, were synthesized, inserted separately into the nonviral eukaryotic expression vector, pcDNA3.1(−), and transfected into MCF-7 cells. Analyses showed that the
HER-2
mRNA and p185, as well as oncogene
k-ras
were down-regulated remarkably in the ribozyme-transfected cells, while the onco-suppressor gene,
p53
, was up-regulated. Furthermore, the tumorigenicity of the RZ1-stably transfected MCF-7 cells was decreased dramatically in nude mice. These results demonstrate that the use of anti-
HER-2
ribozymes may be a beneficial strategy for gene therapy of breast cancer.</description><subject>Adenocarcinoma - therapy</subject><subject>Animal Anatomy</subject><subject>Animal Biochemistry</subject><subject>Animals</subject><subject>Biomedical and Life Sciences</subject><subject>Blotting, Western</subject><subject>Breast cancer</subject><subject>Breast Neoplasms - therapy</subject><subject>Cell Line, Tumor</subject><subject>DNA Primers - genetics</subject><subject>Female</subject><subject>Flow Cytometry</subject><subject>Gene expression</subject><subject>Gene Expression Regulation, Neoplastic - genetics</subject><subject>Gene Targeting - methods</subject><subject>Gene therapy</subject><subject>Genetic Therapy - methods</subject><subject>Genetic Vectors - genetics</subject><subject>Genotype & phenotype</subject><subject>Histology</subject><subject>Humans</subject><subject>Life Sciences</subject><subject>Mice</subject><subject>Mice, Nude</subject><subject>Morphology</subject><subject>Oncology</subject><subject>Proteins</subject><subject>Receptor, ErbB-2 - genetics</subject><subject>Receptor, ErbB-2 - metabolism</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><subject>RNA, Catalytic - genetics</subject><subject>RNA, Catalytic - pharmacology</subject><subject>Transfection</subject><issn>0301-4851</issn><issn>1573-4978</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNqFkc9qFTEUh0OxtNfqA3QjwU3rIvUkOclMlqVWWygKouAuJJnc65Q7f0xmkPYJuu4j-iSm3AstBXEVSL7zyznnI-SQwwkHqN5nzkFKBmCYUdow3CELrirJ0FT1C7IACZxhrfg-eZnzNQAgr9Qe2ecGETXigvwYw4fPp_KEH_-5u3_Huti0booNTa0fbm-6SCeXVnFq-xUdlvTi_CsTNM_jmGLOMVOfossTDa4PMdFp7oZEV2n4Pf18RXaXbp3j6-15QL5_PP92dsGuvny6PDu9YgFBTMx4XYdQR5TeSCHqqhblRgNWlfKh9C6EaUyUeqk16qCdFk1QwrkGlJfeywNytMkd0_BrjnmyXZtDXK9dH4c52wqVASg7-D8ppZGaK1XIt8_I62FOfRnDclMjghKyQHwDhTTknOLSjqntXLqxHOyDHrvRY4se-6DHYql5sw2efVn1Y8XWRwHEBsjlqV_F9OTnf6b-BS-amMo</recordid><startdate>20100301</startdate><enddate>20100301</enddate><creator>He, Pei</creator><creator>Zhu, Dan</creator><creator>Hu, Jun-Jian</creator><creator>Peng, Ju</creator><creator>Chen, Lian-Sheng</creator><creator>Lu, Guang-Xiu</creator><general>Springer Netherlands</general><general>Springer Nature B.V</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7TK</scope><scope>7TM</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>88I</scope><scope>8AO</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>RC3</scope><scope>7X8</scope><scope>7QO</scope><scope>7TO</scope><scope>H94</scope></search><sort><creationdate>20100301</creationdate><title>pcDNA3.1(−)-mediated ribozyme targeting of HER-2 suppresses breast cancer tumor growth</title><author>He, Pei ; Zhu, Dan ; Hu, Jun-Jian ; Peng, Ju ; Chen, Lian-Sheng ; Lu, Guang-Xiu</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c402t-9b68cc8e43b93228782b68604775bc485229d9e36f6646c6a62dc52aad05b3bb3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2010</creationdate><topic>Adenocarcinoma - therapy</topic><topic>Animal Anatomy</topic><topic>Animal Biochemistry</topic><topic>Animals</topic><topic>Biomedical and Life Sciences</topic><topic>Blotting, Western</topic><topic>Breast cancer</topic><topic>Breast Neoplasms - therapy</topic><topic>Cell Line, Tumor</topic><topic>DNA Primers - genetics</topic><topic>Female</topic><topic>Flow Cytometry</topic><topic>Gene expression</topic><topic>Gene Expression Regulation, Neoplastic - genetics</topic><topic>Gene Targeting - methods</topic><topic>Gene therapy</topic><topic>Genetic Therapy - methods</topic><topic>Genetic Vectors - genetics</topic><topic>Genotype & phenotype</topic><topic>Histology</topic><topic>Humans</topic><topic>Life Sciences</topic><topic>Mice</topic><topic>Mice, Nude</topic><topic>Morphology</topic><topic>Oncology</topic><topic>Proteins</topic><topic>Receptor, ErbB-2 - genetics</topic><topic>Receptor, ErbB-2 - metabolism</topic><topic>Reverse Transcriptase Polymerase Chain Reaction</topic><topic>RNA, Catalytic - genetics</topic><topic>RNA, Catalytic - pharmacology</topic><topic>Transfection</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>He, Pei</creatorcontrib><creatorcontrib>Zhu, Dan</creatorcontrib><creatorcontrib>Hu, Jun-Jian</creatorcontrib><creatorcontrib>Peng, Ju</creatorcontrib><creatorcontrib>Chen, Lian-Sheng</creatorcontrib><creatorcontrib>Lu, Guang-Xiu</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Science Database</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central Basic</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>Biotechnology Research Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><jtitle>Molecular biology reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>He, Pei</au><au>Zhu, Dan</au><au>Hu, Jun-Jian</au><au>Peng, Ju</au><au>Chen, Lian-Sheng</au><au>Lu, Guang-Xiu</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>pcDNA3.1(−)-mediated ribozyme targeting of HER-2 suppresses breast cancer tumor growth</atitle><jtitle>Molecular biology reports</jtitle><stitle>Mol Biol Rep</stitle><addtitle>Mol Biol Rep</addtitle><date>2010-03-01</date><risdate>2010</risdate><volume>37</volume><issue>3</issue><spage>1597</spage><epage>1604</epage><pages>1597-1604</pages><issn>0301-4851</issn><eissn>1573-4978</eissn><abstract>The
HER-2
proto-oncogene (also called c-erbB-2/neu) encodes the protein, p185, which is closely related to the growth and metastasis of adenocarcinoma, and is overexpressed in 25–30% of human breast cancers. In this study, we attempt to reverse the malignant phenotype of the breast cancer cell line, MCF-7, using a
HER-2
-specific hammerhead ribozyme. Two anti-
HER-2
hammerhead ribozymes, RZ1 and RZ2, were synthesized, inserted separately into the nonviral eukaryotic expression vector, pcDNA3.1(−), and transfected into MCF-7 cells. Analyses showed that the
HER-2
mRNA and p185, as well as oncogene
k-ras
were down-regulated remarkably in the ribozyme-transfected cells, while the onco-suppressor gene,
p53
, was up-regulated. Furthermore, the tumorigenicity of the RZ1-stably transfected MCF-7 cells was decreased dramatically in nude mice. These results demonstrate that the use of anti-
HER-2
ribozymes may be a beneficial strategy for gene therapy of breast cancer.</abstract><cop>Dordrecht</cop><pub>Springer Netherlands</pub><pmid>19444644</pmid><doi>10.1007/s11033-009-9569-4</doi><tpages>8</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0301-4851 |
| ispartof | Molecular biology reports, 2010-03, Vol.37 (3), p.1597-1604 |
| issn | 0301-4851 1573-4978 |
| language | eng |
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| source | MEDLINE; SpringerLink Journals |
| subjects | Adenocarcinoma - therapy Animal Anatomy Animal Biochemistry Animals Biomedical and Life Sciences Blotting, Western Breast cancer Breast Neoplasms - therapy Cell Line, Tumor DNA Primers - genetics Female Flow Cytometry Gene expression Gene Expression Regulation, Neoplastic - genetics Gene Targeting - methods Gene therapy Genetic Therapy - methods Genetic Vectors - genetics Genotype & phenotype Histology Humans Life Sciences Mice Mice, Nude Morphology Oncology Proteins Receptor, ErbB-2 - genetics Receptor, ErbB-2 - metabolism Reverse Transcriptase Polymerase Chain Reaction RNA, Catalytic - genetics RNA, Catalytic - pharmacology Transfection |
| title | pcDNA3.1(−)-mediated ribozyme targeting of HER-2 suppresses breast cancer tumor growth |
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