Gamma-Irradiation and Doxorubicin Treatment of Normal Human Cells Cause Cell Cycle Arrest Via Different Pathways

Ionizing radiation and doxorubicin both produce oxidative damage and double-strand breaks in DNA. Double-strand breaks and oxidative damage are highly toxic and cause cell cycle arrest, provoking DNA repair and apoptosis in cancer cell lines. To investigate the response of normal human cells to agen...

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Bibliographic Details
Published in:Molecules and cells 2005, 20(3), , pp.331-338
Main Authors: Lee, S.M. (Korea University, Seoul, Republic of Korea), Youn, B.H. (Washington State University, Pullman, WA, USA), Kim, C.S. (Radiation and Health Research Institute, Seoul, Republic of Korea), Kim, C.S. (Korea University, Seoul, Republic of Korea), Kim, J. (Korea University, Seoul, Republic of Korea), E-mail: joonkim@korea.ac.kr, Kang, C.H. (Washington State University, Pullman, WA, USA)
Format: Article
Language:English
Subjects:
ANTIBIOTICOS
ANTIBIOTICS
Antibiotics, Antineoplastic - toxicity
ANTIBIOTIQUE
Biomarkers - metabolism
Cell Cycle - drug effects
Cell Cycle - radiation effects
Differential Gene Expression
DNA Damage - drug effects
DNA Damage - radiation effects
Doxorubicin - toxicity
Fibroblasts - cytology
Fibroblasts - drug effects
Fibroblasts - radiation effects
GAMMA IRRADIATION
Gamma Rays
Gene Expression Profiling
Humans
IRRADIACION GAMMA
IRRADIATION GAMMA
Male
Normal Human Fibroblasts
Oligonucleotide Array Sequence Analysis
Signal Transduction - drug effects
Signal Transduction - radiation effects
생물학
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Summary:Ionizing radiation and doxorubicin both produce oxidative damage and double-strand breaks in DNA. Double-strand breaks and oxidative damage are highly toxic and cause cell cycle arrest, provoking DNA repair and apoptosis in cancer cell lines. To investigate the response of normal human cells to agents causing oxidative damage, we monitored alterations in gene expression in F65 normal human fibroblasts. Treatment with γ-irradiation and doxorubicin altered the expression of 23 and 68 known genes, respectively, with no genes in common. Both agents altered the expression of genes involved in cell cycle arrest, and arrested the treated cells in G₂/M phase 12 h after treatment. 24 h after γ-irradiation, the percentage of G₁ cells increased, whereas after doxorubicin treatment the percentage of G₂/M cells remained constant for 24 h.
ISSN:1016-8478
0219-1032
DOI:10.1016/S1016-8478(23)13235-3