Cell cycle inhibitor, p19INK4d, promotes cell survival and decreases chromosomal aberrations after genotoxic insult due to enhanced DNA repair

Genome integrity and cell proliferation and survival are regulated by an intricate network of pathways that includes cell cycle checkpoints, DNA repair and recombination, and programmed cell death. It makes sense that there should be a coordinated regulation of these different processes, but the com...

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Autores principales:	Scassa, María Elida, Marazita, Mariela C., Ceruti, Julieta María, Carcagno, Abel Luis, González Cid, Marcela Beatriz, Pignataro, Omar Pedro, Cánepa, Eduardo Tomás
Publicado:	2007
Materias:	Apoptosis Cell survival Chromosomal aberrations DNA repair Genotoxic p19INK4d complementary DNA cyclin dependent kinase inhibitor 2D phosphorus 32 RNA animal cell article cell cycle cell growth cell viability chromosome aberration clonogenic assay controlled study DNA damage DNA recombination DNA synthesis flow cytometry genotoxicity growth inhibition isotope labeling mouse nonhuman Northern blotting polyacrylamide gel electrophoresis priority journal protein content tumor cell culture ultraviolet irradiation Western blotting Animals Blotting, Northern Blotting, Western Cell Survival Chromosome Aberrations Colony-Forming Units Assay Cyclin-Dependent Kinase Inhibitor p19 DNA Damage DNA Repair Genomic Instability Humans Immunoprecipitation Mice Pyrimidine Dimers Radiation Tolerance RNA, Messenger Thymidine Ultraviolet Rays
Acceso en línea:	https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_15687864_v6_n5_p626_Scassa http://hdl.handle.net/20.500.12110/paper_15687864_v6_n5_p626_Scassa
Aporte de:	Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA) de Universidad de Buenos Aires

id	paper:paper_15687864_v6_n5_p626_Scassa
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spelling	paper:paper_15687864_v6_n5_p626_Scassa2023-06-08T16:24:09Z Cell cycle inhibitor, p19INK4d, promotes cell survival and decreases chromosomal aberrations after genotoxic insult due to enhanced DNA repair Scassa, María Elida Marazita, Mariela C. Ceruti, Julieta María Carcagno, Abel Luis González Cid, Marcela Beatriz Pignataro, Omar Pedro Cánepa, Eduardo Tomás Apoptosis Cell survival Chromosomal aberrations DNA repair Genotoxic p19INK4d complementary DNA cyclin dependent kinase inhibitor 2D phosphorus 32 RNA animal cell article cell cycle cell growth cell viability chromosome aberration clonogenic assay controlled study DNA damage DNA recombination DNA repair DNA synthesis flow cytometry genotoxicity growth inhibition isotope labeling mouse nonhuman Northern blotting polyacrylamide gel electrophoresis priority journal protein content tumor cell culture ultraviolet irradiation Western blotting Animals Blotting, Northern Blotting, Western Cell Survival Chromosome Aberrations Colony-Forming Units Assay Cyclin-Dependent Kinase Inhibitor p19 DNA Damage DNA Repair Genomic Instability Humans Immunoprecipitation Mice Pyrimidine Dimers Radiation Tolerance RNA, Messenger Thymidine Ultraviolet Rays Genome integrity and cell proliferation and survival are regulated by an intricate network of pathways that includes cell cycle checkpoints, DNA repair and recombination, and programmed cell death. It makes sense that there should be a coordinated regulation of these different processes, but the components of such mechanisms remain unknown. In this report, we demonstrate that p19INK4d expression enhances cell survival under genotoxic conditions. By using p19INK4d-overexpressing clones, we demonstrated that p19INK4d expression correlates with the cellular resistance to UV treatment with increased DNA repair activity against UV-induced lesions. On the contrary, cells transfected with p19INK4d antisense cDNA show reduced ability to repair DNA damage and increased sensitivity to genotoxic insult when compared with their p19INK4d-overexpressing counterparts. Consistent with these findings, our studies also show that p19INK4d-overexpressing cells present not only a minor accumulation of UV-induced chromosomal aberrations but a lower frequency of spontaneous chromosome abnormalities than p19INK4d-antisense cells. Lastly, we suggest that p19INK4d effects are dissociated from its role as CDK4/6 inhibitor. The results presented herein support a crucial role for p19INK4d in regulating genomic stability and overall cell viability under conditions of genotoxic stress. We propose that p19INK4d would belong to a protein network that would integrate DNA repair, apoptotic and checkpoint mechanisms in order to maintain the genomic integrity. © 2007 Elsevier B.V. All rights reserved. Fil:Scassa, M.E. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. Fil:Marazita, M.C. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. Fil:Ceruti, J.M. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. Fil:Carcagno, A.L. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. Fil:González-Cid, M. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. Fil:Pignataro, O.P. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. Fil:Cánepa, E.T. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. 2007 https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_15687864_v6_n5_p626_Scassa http://hdl.handle.net/20.500.12110/paper_15687864_v6_n5_p626_Scassa
institution	Universidad de Buenos Aires
institution_str	I-28
repository_str	R-134
collection	Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA)
topic	Apoptosis Cell survival Chromosomal aberrations DNA repair Genotoxic p19INK4d complementary DNA cyclin dependent kinase inhibitor 2D phosphorus 32 RNA animal cell article cell cycle cell growth cell viability chromosome aberration clonogenic assay controlled study DNA damage DNA recombination DNA repair DNA synthesis flow cytometry genotoxicity growth inhibition isotope labeling mouse nonhuman Northern blotting polyacrylamide gel electrophoresis priority journal protein content tumor cell culture ultraviolet irradiation Western blotting Animals Blotting, Northern Blotting, Western Cell Survival Chromosome Aberrations Colony-Forming Units Assay Cyclin-Dependent Kinase Inhibitor p19 DNA Damage DNA Repair Genomic Instability Humans Immunoprecipitation Mice Pyrimidine Dimers Radiation Tolerance RNA, Messenger Thymidine Ultraviolet Rays
spellingShingle	Apoptosis Cell survival Chromosomal aberrations DNA repair Genotoxic p19INK4d complementary DNA cyclin dependent kinase inhibitor 2D phosphorus 32 RNA animal cell article cell cycle cell growth cell viability chromosome aberration clonogenic assay controlled study DNA damage DNA recombination DNA repair DNA synthesis flow cytometry genotoxicity growth inhibition isotope labeling mouse nonhuman Northern blotting polyacrylamide gel electrophoresis priority journal protein content tumor cell culture ultraviolet irradiation Western blotting Animals Blotting, Northern Blotting, Western Cell Survival Chromosome Aberrations Colony-Forming Units Assay Cyclin-Dependent Kinase Inhibitor p19 DNA Damage DNA Repair Genomic Instability Humans Immunoprecipitation Mice Pyrimidine Dimers Radiation Tolerance RNA, Messenger Thymidine Ultraviolet Rays Scassa, María Elida Marazita, Mariela C. Ceruti, Julieta María Carcagno, Abel Luis González Cid, Marcela Beatriz Pignataro, Omar Pedro Cánepa, Eduardo Tomás Cell cycle inhibitor, p19INK4d, promotes cell survival and decreases chromosomal aberrations after genotoxic insult due to enhanced DNA repair
topic_facet	Apoptosis Cell survival Chromosomal aberrations DNA repair Genotoxic p19INK4d complementary DNA cyclin dependent kinase inhibitor 2D phosphorus 32 RNA animal cell article cell cycle cell growth cell viability chromosome aberration clonogenic assay controlled study DNA damage DNA recombination DNA repair DNA synthesis flow cytometry genotoxicity growth inhibition isotope labeling mouse nonhuman Northern blotting polyacrylamide gel electrophoresis priority journal protein content tumor cell culture ultraviolet irradiation Western blotting Animals Blotting, Northern Blotting, Western Cell Survival Chromosome Aberrations Colony-Forming Units Assay Cyclin-Dependent Kinase Inhibitor p19 DNA Damage DNA Repair Genomic Instability Humans Immunoprecipitation Mice Pyrimidine Dimers Radiation Tolerance RNA, Messenger Thymidine Ultraviolet Rays
description	Genome integrity and cell proliferation and survival are regulated by an intricate network of pathways that includes cell cycle checkpoints, DNA repair and recombination, and programmed cell death. It makes sense that there should be a coordinated regulation of these different processes, but the components of such mechanisms remain unknown. In this report, we demonstrate that p19INK4d expression enhances cell survival under genotoxic conditions. By using p19INK4d-overexpressing clones, we demonstrated that p19INK4d expression correlates with the cellular resistance to UV treatment with increased DNA repair activity against UV-induced lesions. On the contrary, cells transfected with p19INK4d antisense cDNA show reduced ability to repair DNA damage and increased sensitivity to genotoxic insult when compared with their p19INK4d-overexpressing counterparts. Consistent with these findings, our studies also show that p19INK4d-overexpressing cells present not only a minor accumulation of UV-induced chromosomal aberrations but a lower frequency of spontaneous chromosome abnormalities than p19INK4d-antisense cells. Lastly, we suggest that p19INK4d effects are dissociated from its role as CDK4/6 inhibitor. The results presented herein support a crucial role for p19INK4d in regulating genomic stability and overall cell viability under conditions of genotoxic stress. We propose that p19INK4d would belong to a protein network that would integrate DNA repair, apoptotic and checkpoint mechanisms in order to maintain the genomic integrity. © 2007 Elsevier B.V. All rights reserved.
author	Scassa, María Elida Marazita, Mariela C. Ceruti, Julieta María Carcagno, Abel Luis González Cid, Marcela Beatriz Pignataro, Omar Pedro Cánepa, Eduardo Tomás
author_facet	Scassa, María Elida Marazita, Mariela C. Ceruti, Julieta María Carcagno, Abel Luis González Cid, Marcela Beatriz Pignataro, Omar Pedro Cánepa, Eduardo Tomás
author_sort	Scassa, María Elida
title	Cell cycle inhibitor, p19INK4d, promotes cell survival and decreases chromosomal aberrations after genotoxic insult due to enhanced DNA repair
title_short	Cell cycle inhibitor, p19INK4d, promotes cell survival and decreases chromosomal aberrations after genotoxic insult due to enhanced DNA repair
title_full	Cell cycle inhibitor, p19INK4d, promotes cell survival and decreases chromosomal aberrations after genotoxic insult due to enhanced DNA repair
title_fullStr	Cell cycle inhibitor, p19INK4d, promotes cell survival and decreases chromosomal aberrations after genotoxic insult due to enhanced DNA repair
title_full_unstemmed	Cell cycle inhibitor, p19INK4d, promotes cell survival and decreases chromosomal aberrations after genotoxic insult due to enhanced DNA repair
title_sort	cell cycle inhibitor, p19ink4d, promotes cell survival and decreases chromosomal aberrations after genotoxic insult due to enhanced dna repair
publishDate	2007
url	https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_15687864_v6_n5_p626_Scassa http://hdl.handle.net/20.500.12110/paper_15687864_v6_n5_p626_Scassa
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Cell cycle inhibitor, p19INK4d, promotes cell survival and decreases chromosomal aberrations after genotoxic insult due to enhanced DNA repair

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