DNA mismatch repair protein MSH2 dictates cellular survival in response to low dose radiation in endometrial carcinoma cells.
AuthorsMartin, Lynn M
Davies, Anthony M
Lynch, Thomas H
AffiliationRadiation and Urologic Oncology, Prostate Molecular Oncology Research Group, Academic Unit of Clinical and Molecular Oncology, Institute of Molecular Medicine, Trinity College Dublin, Dublin 8, Ireland.
Local subject classificationCELL BIOLOGY
Cell Line, Tumor
DNA Mismatch Repair
G2 Phase Cell Cycle Checkpoints
MutS Homolog 2 Protein
Recombinational DNA Repair
MetadataShow full item record
CitationMartin LM et al. DNA mismatch repair protein MSH2 dictates cellular survival in response to low dose radiation in endometrial carcinoma cells. 2013, 335 (1):19-25 Cancer Lett.
PublisherElsevier Ireland Ltd
AbstractDNA repair and G2-phase cell cycle checkpoint responses are involved in the manifestation of hyper-radiosensitivity (HRS). The low-dose radioresponse of MSH2 isogenic endometrial carcinoma cell lines was examined. Defects in cell cycle checkpoint activation and the DNA damage response in irradiated cells (0.2 Gy) were evaluated. HRS was expressed solely in MSH2+ cells and was associated with efficient activation of the early G2-phase cell cycle checkpoint. Maintenance of the arrest was associated with persistent MRE11, γH2AX, RAD51 foci at 2 h after irradiation. Persistent MRE11 and RAD51 foci were also evident 24 h after 0.2 Gy. MSH2 significantly enhances cell radiosensitivity to low dose IR.