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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Veröffentlicht in:Radiation research 2004-05, Vol.161 (5), p.504-510
Hauptverfasser: Franken, N. A P., van Bree, C., Haveman, J.
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Haveman, J.
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.
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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. 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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. 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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. 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source MEDLINE; BioOne Complete; Jstor Complete Legacy
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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