Evaluation of Adaptive Responses to Cisplatin in Normal and Mutant Cell Lines with Mutations in Recombination Repair Pathways

Cell lines mutant in specific DNA repair pathways were used to determine if these pathways are involved in adaptive responses. For these studies, the effect of deficiencies in homologous recombination repair (HR) were studied in the parental AA8 and mutant irs ISF cell line pair and for deficiencies...

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Bibliographic Details
Published in:Anticancer research 2006-03, Vol.26 (2A), p.1183-1187
Main Authors: RAAPHORST, G. P, LI, L. F, YANG, D. P
Format: Article
Language:English
Subjects:
Animals
Antigens, Nuclear - genetics
Antineoplastic Agents - pharmacology
Biological and medical sciences
Cell Line
CHO Cells
Cisplatin - pharmacology
Cricetinae
DNA Repair - genetics
DNA Repair - physiology
DNA-Binding Proteins - genetics
Embryo, Mammalian
Fibroblasts
Ku Autoantigen
Medical sciences
Mice
Mice, Knockout
Mutation
Recombination, Genetic - genetics
Tumors
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Summary:Cell lines mutant in specific DNA repair pathways were used to determine if these pathways are involved in adaptive responses. For these studies, the effect of deficiencies in homologous recombination repair (HR) were studied in the parental AA8 and mutant irs ISF cell line pair and for deficiencies in the nonhomologous endjoining (NHEJ) pathway in the mouse MEF parental and Ku80 mutant cell line pair. The results showed that the XRCC3 mutation in the HR-deficient mutant inhibited adaptive responses to low doses of cisplatin and radiation. The parental lines showed transient adaptive responses to both low-dose cisplatin and radiation treatment. For the mouse MEF and the Ku80 cells, no adaptive responses were observed in either cell line. However, there was an initial transient sensitization response followed by partial recovery. Thus, it appears that the HR repair system may be involved in the adaptive response to cisplatin and radiation. For the NHEJ repair system the question could not be answered since no adaptive responses were evident in the parental line.
ISSN:0250-7005
1791-7530