Depletion of KIN17, a Human DNA Replication Protein, Increases the Radiosensitivity of RKO Cells

Despras, E., Miccoli, L., Créminon, C., Rouillard, D., Angulo, J. F. and Biard, D. S. F. Depletion of KIN17, a Human DNA Replication Protein, Increases the Radiosensitivity of RKO Cells. Radiat. Res. 159, 748–758 (2003). The human KIN17 protein is a chromatin-associated protein involved in DNA repli...

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Veröffentlicht in:Radiation research 2003-06, Vol.159 (6), p.748-758
Hauptverfasser: Despras, E., Miccoli, L., Créminon, C., Rouillard, D., Angulo, J. F., Biard, D. S F.
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container_end_page 758
container_issue 6
container_start_page 748
container_title Radiation research
container_volume 159
creator Despras, E.
Miccoli, L.
Créminon, C.
Rouillard, D.
Angulo, J. F.
Biard, D. S F.
description Despras, E., Miccoli, L., Créminon, C., Rouillard, D., Angulo, J. F. and Biard, D. S. F. Depletion of KIN17, a Human DNA Replication Protein, Increases the Radiosensitivity of RKO Cells. Radiat. Res. 159, 748–758 (2003). The human KIN17 protein is a chromatin-associated protein involved in DNA replication. Certain tumor cell lines overproduce KIN17 protein. Among 16 cell lines, the highest KIN17 protein level was observed in H1299 non-small cell lung cancer cells, whereas the lowest was detected in MeWo melanoma cells. Cells displaying higher KIN17 protein levels exhibited elevated RPA70 protein contents. High KIN17 protein levels may be a consequence of the tumorigenic phenotype or a prerequisite for tumor progression. Twenty-four hours after exposure to ionizing radiation, after the completion of DNA repair, a co-induction of chromatin-bound KIN17 and RPA70 proteins was detected. Etoposide, an inhibitor of topoisomerase II generating double-strand breaks, triggered the concentration of KIN17 into punctuate intranuclear foci. KIN17 may be associated with unrepaired DNA sites. Flow cytometry analysis revealed that 48 h after transfection the uppermost KIN17-positive RKO cells shifted in the cell cycle toward higher DNA content, suggesting that KIN17 protein induced defects in chromatin conformation. Cells displaying reduced levels of KIN17 transcript exhibited a sixfold increased radiosensitivity at 2 Gy. The KIN17 protein may be a component of the DNA replication machinery that participates in the cellular response to unrepaired DSBs, and an impaired KIN17 pathway leads to an increased sensitivity to ionizing radiation.
doi_str_mv 10.1667/0033-7587(2003)159[0748:DOKAHD]2.0.CO;2
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F.</creatorcontrib><creatorcontrib>Biard, D. S F.</creatorcontrib><title>Depletion of KIN17, a Human DNA Replication Protein, Increases the Radiosensitivity of RKO Cells</title><title>Radiation research</title><addtitle>Radiat Res</addtitle><description>Despras, E., Miccoli, L., Créminon, C., Rouillard, D., Angulo, J. F. and Biard, D. S. F. Depletion of KIN17, a Human DNA Replication Protein, Increases the Radiosensitivity of RKO Cells. Radiat. Res. 159, 748–758 (2003). The human KIN17 protein is a chromatin-associated protein involved in DNA replication. Certain tumor cell lines overproduce KIN17 protein. Among 16 cell lines, the highest KIN17 protein level was observed in H1299 non-small cell lung cancer cells, whereas the lowest was detected in MeWo melanoma cells. Cells displaying higher KIN17 protein levels exhibited elevated RPA70 protein contents. High KIN17 protein levels may be a consequence of the tumorigenic phenotype or a prerequisite for tumor progression. Twenty-four hours after exposure to ionizing radiation, after the completion of DNA repair, a co-induction of chromatin-bound KIN17 and RPA70 proteins was detected. Etoposide, an inhibitor of topoisomerase II generating double-strand breaks, triggered the concentration of KIN17 into punctuate intranuclear foci. KIN17 may be associated with unrepaired DNA sites. Flow cytometry analysis revealed that 48 h after transfection the uppermost KIN17-positive RKO cells shifted in the cell cycle toward higher DNA content, suggesting that KIN17 protein induced defects in chromatin conformation. Cells displaying reduced levels of KIN17 transcript exhibited a sixfold increased radiosensitivity at 2 Gy. 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Cells displaying higher KIN17 protein levels exhibited elevated RPA70 protein contents. High KIN17 protein levels may be a consequence of the tumorigenic phenotype or a prerequisite for tumor progression. Twenty-four hours after exposure to ionizing radiation, after the completion of DNA repair, a co-induction of chromatin-bound KIN17 and RPA70 proteins was detected. Etoposide, an inhibitor of topoisomerase II generating double-strand breaks, triggered the concentration of KIN17 into punctuate intranuclear foci. KIN17 may be associated with unrepaired DNA sites. Flow cytometry analysis revealed that 48 h after transfection the uppermost KIN17-positive RKO cells shifted in the cell cycle toward higher DNA content, suggesting that KIN17 protein induced defects in chromatin conformation. Cells displaying reduced levels of KIN17 transcript exhibited a sixfold increased radiosensitivity at 2 Gy. The KIN17 protein may be a component of the DNA replication machinery that participates in the cellular response to unrepaired DSBs, and an impaired KIN17 pathway leads to an increased sensitivity to ionizing radiation.</abstract><cop>Oak Brook, Il</cop><pub>Radiation Research Society</pub><pmid>12751957</pmid><doi>10.1667/0033-7587(2003)159[0748:DOKAHD]2.0.CO;2</doi><tpages>11</tpages></addata></record>
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source MEDLINE; BioOne Complete; Jstor Complete Legacy
subjects Animals
Biological and medical sciences
Cell cycle
Cell lines
Cell Nucleus - metabolism
Chromatin - chemistry
DNA
DNA Damage
DNA Replication
DNA-Binding Proteins - analysis
DNA-Binding Proteins - physiology
Enzyme-Linked Immunosorbent Assay
Etoposide - pharmacology
Gamma Rays
HCT116 cells
HEK293 cells
HeLa cells
Humans
K562 cells
Kidney cells
Medical sciences
Mice
Nuclear Proteins
Proteins
Radiation Tolerance
REGULAR ARTICLES
RNA-Binding Proteins
Space life sciences
Tumor Cells, Cultured
title Depletion of KIN17, a Human DNA Replication Protein, Increases the Radiosensitivity of RKO Cells
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