Differential Response to Radiation of TP53-Inactivated Cells by Overexpression of Dominant-Negative Mutant TP53 or HPVE6
Franken, N. A. P., van Bree, C. and Haveman, J. Differential Response to Radiation of TP53-Inactivated Cells by Overexpression of Dominant-Negative Mutant TP53 or HPVE6. Radiat. Res. 161, 504–510 (2004). The inactivation of TP53 by transfection of a dominant- negative mutated TP53 (MP53.13 cells) wa...
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description | Franken, N. A. P., van Bree, C. and Haveman, J. Differential Response to Radiation of TP53-Inactivated Cells by Overexpression of Dominant-Negative Mutant TP53 or HPVE6. Radiat. Res. 161, 504–510 (2004). The inactivation of TP53 by transfection of a dominant- negative mutated TP53 (MP53.13 cells) was compared with inactivation of TP53 by transfection with the HPV E6 gene (RC10.1 cells) with respect to PLD repair, G1-phase arrest, and induction of color junctions. Functional G1 arrest was demonstrated in parental (RKO) cells with wild-type TP53, while in RC10.1 cells the G1 arrest was eliminated. In MP53.13 cells an intermediate G1 arrest was found. Functionality of endogenous TP53 was confirmed in RKO and MP53.13 cells by accumulation of TP53 protein and its downstream target CDKN1A (p21). Radiation survival of MP53.13 cells was higher than that of RKO cells, and PLD repair was found in RKO cells and MP53.13 cells but not in RC10.1 cells. Both with and without irradiation, the number of color junctions was 50 to 80% higher in MP53.13 cells than in RKO and RC10.1 cells. In the MP53.13 cells, the genetic instability appears to lead to more aberrations and to radioresistance. In spite of the presence of an excess of mutated TP53, wild- type TP53 functions appear to be affected only partly or not at all. |
doi_str_mv | 10.1667/RR3160 |
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A P. ; van Bree, C. ; Haveman, J.</creator><creatorcontrib>Franken, N. A P. ; van Bree, C. ; Haveman, J.</creatorcontrib><description>Franken, N. A. P., van Bree, C. and Haveman, J. Differential Response to Radiation of TP53-Inactivated Cells by Overexpression of Dominant-Negative Mutant TP53 or HPVE6. Radiat. Res. 161, 504–510 (2004). The inactivation of TP53 by transfection of a dominant- negative mutated TP53 (MP53.13 cells) was compared with inactivation of TP53 by transfection with the HPV E6 gene (RC10.1 cells) with respect to PLD repair, G1-phase arrest, and induction of color junctions. Functional G1 arrest was demonstrated in parental (RKO) cells with wild-type TP53, while in RC10.1 cells the G1 arrest was eliminated. In MP53.13 cells an intermediate G1 arrest was found. Functionality of endogenous TP53 was confirmed in RKO and MP53.13 cells by accumulation of TP53 protein and its downstream target CDKN1A (p21). Radiation survival of MP53.13 cells was higher than that of RKO cells, and PLD repair was found in RKO cells and MP53.13 cells but not in RC10.1 cells. Both with and without irradiation, the number of color junctions was 50 to 80% higher in MP53.13 cells than in RKO and RC10.1 cells. In the MP53.13 cells, the genetic instability appears to lead to more aberrations and to radioresistance. In spite of the presence of an excess of mutated TP53, wild- type TP53 functions appear to be affected only partly or not at all.</description><identifier>ISSN: 0033-7587</identifier><identifier>EISSN: 1938-5404</identifier><identifier>DOI: 10.1667/RR3160</identifier><identifier>PMID: 15161374</identifier><language>eng</language><publisher>United States: Radiation Research Society</publisher><subject>Cell culture techniques ; Cell cycle ; Cell lines ; Cell Survival - radiation effects ; Chromosome Aberrations ; Chromosomes ; Chromosomes, Human - radiation effects ; Colorectal Neoplasms - genetics ; Colorectal Neoplasms - metabolism ; Colorectal Neoplasms - pathology ; Cultured cells ; Dose-Response Relationship, Radiation ; Embryonic cells ; Gene Expression Regulation, Neoplastic - radiation effects ; Gene Silencing ; Humans ; Ionizing radiation ; Irradiation ; Metaphase - radiation effects ; Mutation ; Oncogene Proteins, Viral - genetics ; Oncogene Proteins, Viral - metabolism ; Radiation Dosage ; Radiation tolerance ; Radiotherapy ; Recombinant Proteins - metabolism ; REGULAR ARTICLES ; Repressor Proteins ; Tumor Suppressor Protein p53 - genetics ; Tumor Suppressor Protein p53 - metabolism</subject><ispartof>Radiation research, 2004-05, Vol.161 (5), p.504-510</ispartof><rights>Radiation Research Society</rights><rights>Copyright 2004 The Radiation Research Society</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-b391t-9dee680ad736b1f687da36dde9631464232d809b5e7ec9577b514ff7569088033</citedby><cites>FETCH-LOGICAL-b391t-9dee680ad736b1f687da36dde9631464232d809b5e7ec9577b514ff7569088033</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://bioone.org/doi/pdf/10.1667/RR3160$$EPDF$$P50$$Gbioone$$H</linktopdf><linktohtml>$$Uhttps://www.jstor.org/stable/3581262$$EHTML$$P50$$Gjstor$$H</linktohtml><link.rule.ids>314,776,780,799,26957,27903,27904,52341,57995,58228</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15161374$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Franken, N. A P.</creatorcontrib><creatorcontrib>van Bree, C.</creatorcontrib><creatorcontrib>Haveman, J.</creatorcontrib><title>Differential Response to Radiation of TP53-Inactivated Cells by Overexpression of Dominant-Negative Mutant TP53 or HPVE6</title><title>Radiation research</title><addtitle>Radiat Res</addtitle><description>Franken, N. A. P., van Bree, C. and Haveman, J. Differential Response to Radiation of TP53-Inactivated Cells by Overexpression of Dominant-Negative Mutant TP53 or HPVE6. Radiat. Res. 161, 504–510 (2004). The inactivation of TP53 by transfection of a dominant- negative mutated TP53 (MP53.13 cells) was compared with inactivation of TP53 by transfection with the HPV E6 gene (RC10.1 cells) with respect to PLD repair, G1-phase arrest, and induction of color junctions. Functional G1 arrest was demonstrated in parental (RKO) cells with wild-type TP53, while in RC10.1 cells the G1 arrest was eliminated. In MP53.13 cells an intermediate G1 arrest was found. Functionality of endogenous TP53 was confirmed in RKO and MP53.13 cells by accumulation of TP53 protein and its downstream target CDKN1A (p21). Radiation survival of MP53.13 cells was higher than that of RKO cells, and PLD repair was found in RKO cells and MP53.13 cells but not in RC10.1 cells. Both with and without irradiation, the number of color junctions was 50 to 80% higher in MP53.13 cells than in RKO and RC10.1 cells. In the MP53.13 cells, the genetic instability appears to lead to more aberrations and to radioresistance. In spite of the presence of an excess of mutated TP53, wild- type TP53 functions appear to be affected only partly or not at all.</description><subject>Cell culture techniques</subject><subject>Cell cycle</subject><subject>Cell lines</subject><subject>Cell Survival - radiation effects</subject><subject>Chromosome Aberrations</subject><subject>Chromosomes</subject><subject>Chromosomes, Human - radiation effects</subject><subject>Colorectal Neoplasms - genetics</subject><subject>Colorectal Neoplasms - metabolism</subject><subject>Colorectal Neoplasms - pathology</subject><subject>Cultured cells</subject><subject>Dose-Response Relationship, Radiation</subject><subject>Embryonic cells</subject><subject>Gene Expression Regulation, Neoplastic - radiation effects</subject><subject>Gene Silencing</subject><subject>Humans</subject><subject>Ionizing radiation</subject><subject>Irradiation</subject><subject>Metaphase - radiation effects</subject><subject>Mutation</subject><subject>Oncogene Proteins, Viral - genetics</subject><subject>Oncogene Proteins, Viral - metabolism</subject><subject>Radiation Dosage</subject><subject>Radiation tolerance</subject><subject>Radiotherapy</subject><subject>Recombinant Proteins - metabolism</subject><subject>REGULAR ARTICLES</subject><subject>Repressor Proteins</subject><subject>Tumor Suppressor Protein p53 - genetics</subject><subject>Tumor Suppressor Protein p53 - metabolism</subject><issn>0033-7587</issn><issn>1938-5404</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kFFPwjAUhRujEUT9Bcb0wfg2bde1XR8NoJCgkAV9XTp6Z0bGuqyFwL93OqJPPt2cnO-em3sQuqbkgQohH5OEUUFOUJ8qFgc8ItEp6hPCWCB5LHvowrk1aTUV6hz1KKeCMhn10X5U5Dk0UPlClzgBV9vKAfYWJ9oU2he2wjbHywVnwbTSK1_stAeDh1CWDmcHPN-12_u6AeeO7MhuikpXPniDzzZgB_h161v9E4JtgyeLj7G4RGe5Lh1cHecAvT-Pl8NJMJu_TIdPsyBjivpAGQARE20kExnNRSyNZsIYUILRSEQhC01MVMZBwkpxKTNOozyXXCgSx-3_A3Tf5a4a61wDeVo3xUY3h5SS9Lu6tKuuBW87sN5mGzB_2LGrFrjpgLXztvn1GY9pKMLWvuvsrLC2gv_OfAFOnHzU</recordid><startdate>200405</startdate><enddate>200405</enddate><creator>Franken, N. A P.</creator><creator>van Bree, C.</creator><creator>Haveman, J.</creator><general>Radiation Research Society</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></search><sort><creationdate>200405</creationdate><title>Differential Response to Radiation of TP53-Inactivated Cells by Overexpression of Dominant-Negative Mutant TP53 or HPVE6</title><author>Franken, N. A P. ; van Bree, C. ; Haveman, J.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-b391t-9dee680ad736b1f687da36dde9631464232d809b5e7ec9577b514ff7569088033</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>Cell culture techniques</topic><topic>Cell cycle</topic><topic>Cell lines</topic><topic>Cell Survival - radiation effects</topic><topic>Chromosome Aberrations</topic><topic>Chromosomes</topic><topic>Chromosomes, Human - radiation effects</topic><topic>Colorectal Neoplasms - genetics</topic><topic>Colorectal Neoplasms - metabolism</topic><topic>Colorectal Neoplasms - pathology</topic><topic>Cultured cells</topic><topic>Dose-Response Relationship, Radiation</topic><topic>Embryonic cells</topic><topic>Gene Expression Regulation, Neoplastic - radiation effects</topic><topic>Gene Silencing</topic><topic>Humans</topic><topic>Ionizing radiation</topic><topic>Irradiation</topic><topic>Metaphase - radiation effects</topic><topic>Mutation</topic><topic>Oncogene Proteins, Viral - genetics</topic><topic>Oncogene Proteins, Viral - metabolism</topic><topic>Radiation Dosage</topic><topic>Radiation tolerance</topic><topic>Radiotherapy</topic><topic>Recombinant Proteins - metabolism</topic><topic>REGULAR ARTICLES</topic><topic>Repressor Proteins</topic><topic>Tumor Suppressor Protein p53 - genetics</topic><topic>Tumor Suppressor Protein p53 - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Franken, N. A P.</creatorcontrib><creatorcontrib>van Bree, C.</creatorcontrib><creatorcontrib>Haveman, J.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><jtitle>Radiation research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Franken, N. A P.</au><au>van Bree, C.</au><au>Haveman, J.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Differential Response to Radiation of TP53-Inactivated Cells by Overexpression of Dominant-Negative Mutant TP53 or HPVE6</atitle><jtitle>Radiation research</jtitle><addtitle>Radiat Res</addtitle><date>2004-05</date><risdate>2004</risdate><volume>161</volume><issue>5</issue><spage>504</spage><epage>510</epage><pages>504-510</pages><issn>0033-7587</issn><eissn>1938-5404</eissn><abstract>Franken, N. A. P., van Bree, C. and Haveman, J. Differential Response to Radiation of TP53-Inactivated Cells by Overexpression of Dominant-Negative Mutant TP53 or HPVE6. Radiat. Res. 161, 504–510 (2004). The inactivation of TP53 by transfection of a dominant- negative mutated TP53 (MP53.13 cells) was compared with inactivation of TP53 by transfection with the HPV E6 gene (RC10.1 cells) with respect to PLD repair, G1-phase arrest, and induction of color junctions. Functional G1 arrest was demonstrated in parental (RKO) cells with wild-type TP53, while in RC10.1 cells the G1 arrest was eliminated. In MP53.13 cells an intermediate G1 arrest was found. Functionality of endogenous TP53 was confirmed in RKO and MP53.13 cells by accumulation of TP53 protein and its downstream target CDKN1A (p21). Radiation survival of MP53.13 cells was higher than that of RKO cells, and PLD repair was found in RKO cells and MP53.13 cells but not in RC10.1 cells. Both with and without irradiation, the number of color junctions was 50 to 80% higher in MP53.13 cells than in RKO and RC10.1 cells. In the MP53.13 cells, the genetic instability appears to lead to more aberrations and to radioresistance. In spite of the presence of an excess of mutated TP53, wild- type TP53 functions appear to be affected only partly or not at all.</abstract><cop>United States</cop><pub>Radiation Research Society</pub><pmid>15161374</pmid><doi>10.1667/RR3160</doi><tpages>7</tpages></addata></record> |
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subjects | Cell culture techniques Cell cycle Cell lines Cell Survival - radiation effects Chromosome Aberrations Chromosomes Chromosomes, Human - radiation effects Colorectal Neoplasms - genetics Colorectal Neoplasms - metabolism Colorectal Neoplasms - pathology Cultured cells Dose-Response Relationship, Radiation Embryonic cells Gene Expression Regulation, Neoplastic - radiation effects Gene Silencing Humans Ionizing radiation Irradiation Metaphase - radiation effects Mutation Oncogene Proteins, Viral - genetics Oncogene Proteins, Viral - metabolism Radiation Dosage Radiation tolerance Radiotherapy Recombinant Proteins - metabolism REGULAR ARTICLES Repressor Proteins Tumor Suppressor Protein p53 - genetics Tumor Suppressor Protein p53 - metabolism |
title | Differential Response to Radiation of TP53-Inactivated Cells by Overexpression of Dominant-Negative Mutant TP53 or HPVE6 |
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