Studying the DNA damage response pathway in hematopoietic canine cancer cell lines, a necessary step for finding targets to generate new therapies to treat cancer in dogs.
ATR
Chk1
Claspin
Rad51
leukemia
lymphoma
Journal
Frontiers in veterinary science
ISSN: 2297-1769
Titre abrégé: Front Vet Sci
Pays: Switzerland
ID NLM: 101666658
Informations de publication
Date de publication:
2023
2023
Historique:
received:
23
05
2023
accepted:
31
07
2023
medline:
1
9
2023
pubmed:
1
9
2023
entrez:
1
9
2023
Statut:
epublish
Résumé
Dogs present a significant opportunity for studies in comparative oncology. However, the study of cancer biology phenomena in canine cells is currently limited by restricted availability of validated antibody reagents and techniques. Here, we provide an initial characterization of the expression and activity of key components of the DNA Damage Response (DDR) in a panel of hematopoietic canine cancer cell lines, with the use of commercially available antibody reagents. The techniques used for this validation analysis were western blot, qPCR, and DNA combing assay. Substantial variations in both the basal expression (ATR, Claspin, Chk1, and Rad51) and agonist-induced activation (p-Chk1) of DDR components were observed in canine cancer cell lines. The expression was stronger in the CLBL-1 (B-cell lymphoma) and CLB70 (B-cell chronic lymphocytic leukemia) cell lines than in the GL-1 (B-cell leukemia) cell line, but the biological significance of these differences requires further investigation. We also validated methodologies for quantifying DNA replication dynamics in hematopoietic canine cancer cell lines, and found that the GL-1 cell line presented a higher replication fork speed than the CLBL-1 cell line, but that both showed a tendency to replication fork asymmetry. These findings will inform future studies on cancer biology, which will facilitate progress in developing novel anticancer therapies for canine patients. They can also provide new knowledge in human oncology.
Sections du résumé
Background
UNASSIGNED
Dogs present a significant opportunity for studies in comparative oncology. However, the study of cancer biology phenomena in canine cells is currently limited by restricted availability of validated antibody reagents and techniques. Here, we provide an initial characterization of the expression and activity of key components of the DNA Damage Response (DDR) in a panel of hematopoietic canine cancer cell lines, with the use of commercially available antibody reagents.
Materials and methods
UNASSIGNED
The techniques used for this validation analysis were western blot, qPCR, and DNA combing assay.
Results
UNASSIGNED
Substantial variations in both the basal expression (ATR, Claspin, Chk1, and Rad51) and agonist-induced activation (p-Chk1) of DDR components were observed in canine cancer cell lines. The expression was stronger in the CLBL-1 (B-cell lymphoma) and CLB70 (B-cell chronic lymphocytic leukemia) cell lines than in the GL-1 (B-cell leukemia) cell line, but the biological significance of these differences requires further investigation. We also validated methodologies for quantifying DNA replication dynamics in hematopoietic canine cancer cell lines, and found that the GL-1 cell line presented a higher replication fork speed than the CLBL-1 cell line, but that both showed a tendency to replication fork asymmetry.
Conclusion
UNASSIGNED
These findings will inform future studies on cancer biology, which will facilitate progress in developing novel anticancer therapies for canine patients. They can also provide new knowledge in human oncology.
Identifiants
pubmed: 37655260
doi: 10.3389/fvets.2023.1227683
pmc: PMC10467447
doi:
Types de publication
Journal Article
Langues
eng
Pagination
1227683Informations de copyright
Copyright © 2023 Hernández-Suárez, Gillespie, Dejnaka, Kupczyk, Obmińska-Mrukowicz and Pawlak.
Déclaration de conflit d'intérêts
The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
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