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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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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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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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. 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.</description><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Cell cycle</subject><subject>Cell lines</subject><subject>Cell Nucleus - metabolism</subject><subject>Chromatin - chemistry</subject><subject>DNA</subject><subject>DNA Damage</subject><subject>DNA Replication</subject><subject>DNA-Binding Proteins - analysis</subject><subject>DNA-Binding Proteins - physiology</subject><subject>Enzyme-Linked Immunosorbent Assay</subject><subject>Etoposide - pharmacology</subject><subject>Gamma Rays</subject><subject>HCT116 cells</subject><subject>HEK293 cells</subject><subject>HeLa cells</subject><subject>Humans</subject><subject>K562 cells</subject><subject>Kidney cells</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Nuclear Proteins</subject><subject>Proteins</subject><subject>Radiation Tolerance</subject><subject>REGULAR ARTICLES</subject><subject>RNA-Binding Proteins</subject><subject>Space life sciences</subject><subject>Tumor Cells, Cultured</subject><issn>0033-7587</issn><issn>1938-5404</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqdkF1v0zAUhi0EYmXjHyDkGxBIS-fP2GZXVTrWqtOCKrhCyDiOIzylcRenSPv3OKTa7ndlW-_j9xw9AFxgNMd5Li4QojQTXIpPJF0_Y65-IsHkl2W5WayWv8gczYvykrwAM6yozDhD7CWYPf46AW9ivEPpjXP1GpxgIjhWXMzA76Xbt27woYOhgZv1LRbn0MDVYWc6uLxdwG3KvTX_iW99GJzvzuG6s70z0UU4_HFwa2ofouuiH_xfPzyMTdtNCQvXtvEMvGpMG93b43kKfny9-l6sspvyel0sbrKKcTZkjRLEYU4VcrjJGeOyZo2wwjZ5pYSsak4YqqWqbI4qKithqxwzi4VghjrD6Cn4OPXu-3B_cHHQOx9t2sB0LhyiFpQohJhM4PUE2j7E2LtG73u_M_2DxkiPsvWoTY_a9ChbJ9l6lK0n2ZpopItSk9T0_jjyUO1c_dRztJuAD0fARGvapjed9fGJY1LkAo0rvZu4uziE_jGnXGIi8xRfTXHlQ-jcs_f9B5__puw</recordid><startdate>20030601</startdate><enddate>20030601</enddate><creator>Despras, E.</creator><creator>Miccoli, L.</creator><creator>Créminon, C.</creator><creator>Rouillard, D.</creator><creator>Angulo, J. F.</creator><creator>Biard, D. S F.</creator><general>Radiation Research Society</general><scope>IQODW</scope><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>7X8</scope></search><sort><creationdate>20030601</creationdate><title>Depletion of KIN17, a Human DNA Replication Protein, Increases the Radiosensitivity of RKO Cells</title><author>Despras, E. ; Miccoli, L. ; Créminon, C. ; Rouillard, D. ; Angulo, J. F. ; Biard, D. S F.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-b454t-f972e15390e1f64458d4f7c7cf6b978bd5240d89bc60b38b7cb614c1774a3ea43</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2003</creationdate><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Cell cycle</topic><topic>Cell lines</topic><topic>Cell Nucleus - metabolism</topic><topic>Chromatin - chemistry</topic><topic>DNA</topic><topic>DNA Damage</topic><topic>DNA Replication</topic><topic>DNA-Binding Proteins - analysis</topic><topic>DNA-Binding Proteins - physiology</topic><topic>Enzyme-Linked Immunosorbent Assay</topic><topic>Etoposide - pharmacology</topic><topic>Gamma Rays</topic><topic>HCT116 cells</topic><topic>HEK293 cells</topic><topic>HeLa cells</topic><topic>Humans</topic><topic>K562 cells</topic><topic>Kidney cells</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>Nuclear Proteins</topic><topic>Proteins</topic><topic>Radiation Tolerance</topic><topic>REGULAR ARTICLES</topic><topic>RNA-Binding Proteins</topic><topic>Space life sciences</topic><topic>Tumor Cells, Cultured</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Despras, E.</creatorcontrib><creatorcontrib>Miccoli, L.</creatorcontrib><creatorcontrib>Créminon, C.</creatorcontrib><creatorcontrib>Rouillard, D.</creatorcontrib><creatorcontrib>Angulo, J. F.</creatorcontrib><creatorcontrib>Biard, D. S F.</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Radiation research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Despras, E.</au><au>Miccoli, L.</au><au>Créminon, C.</au><au>Rouillard, D.</au><au>Angulo, J. F.</au><au>Biard, D. S F.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Depletion of KIN17, a Human DNA Replication Protein, Increases the Radiosensitivity of RKO Cells</atitle><jtitle>Radiation research</jtitle><addtitle>Radiat Res</addtitle><date>2003-06-01</date><risdate>2003</risdate><volume>159</volume><issue>6</issue><spage>748</spage><epage>758</epage><pages>748-758</pages><issn>0033-7587</issn><eissn>1938-5404</eissn><coden>RAREAE</coden><abstract>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.</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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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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