Determination of the DNA repair pathways utilised by acute lymphoblastic leukaemia cells following daunorubicin treatment

• Main Authors: Hussain Mubarak Al-Aamri, Helen R. Irving, Terri Meehan-Andrews, Christopher Bradley
• Format: Article
• Language: English
• Published: BMC 2019-09-01
• Series: BMC Research Notes
• Subjects: Daunorubicin; DNA double strand breaks (DSBs); Homologous recombination pathway (HR); Non-homologous end joining (NHEJ) pathway
• Online Access: http://link.springer.com/article/10.1186/s13104-019-4663-8

Abstract Objective DNA double strand breaks (DNA-DSBs) are among the most lethal DNA lesions leading to genomic instability and repaired by either homologous recombination (HR) or the non-homologous end joining (NHEJ) mechanisms. The purpose of this study was to assess the importance and the level of activation of non-homologous end joining (NHEJ) and homologous recombination (HR) DNA repair pathways in three cell lines, CCRF-CEM and MOLT-4 derived from T lymphocytes and SUP-B15 derived from B lymphocytes following treatment with chemotherapy agent daunorubicin. Results The Gamma histone H2AX (γH2AX) assay was used assess the effects of DNA-PK inhibitor NU7026 and RAD51 inhibitor RI-2 on repair of DNA-DSB following treatment with daunorubicin. In all cell lines, the NHEJ DNA repair pathway appeared more rapid and efficient. MOLT-4 and CCFR-CEM cells utilised both NHEJ and HR pathways for DNA-DSB repair. Whereas, SUP-B15 cells utilised only NHEJ for DSB repair, suggestive of a deficiency in HR repair pathways.