DNA mismatch repair protein MSH2 dictates cellular survival in response to low dose radiation in endometrial carcinoma cells.

Thumbnail
Name:
Publisher version
Authors
Martin, Lynn M
Marples, Brian
Davies, Anthony M
Atzberger, Ann
Edwards, Connla
Lynch, Thomas H
Hollywood, Donal
Marignol, Laure
Affiliation
Radiation 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.
Issue Date
2013-07-10
Keywords
CANCER
Local subject classification
CELL BIOLOGY
MeSH
Carcinoma
Cell Line, Tumor
Cell Nucleus
Cell Survival
DNA Mismatch Repair
DNA-Binding Proteins
Endometrial Neoplasms
Female
G2 Phase Cell Cycle Checkpoints
Gene Expression
Histones
Humans
MutS Homolog 2 Protein
Radiation Tolerance
Recombinational DNA Repair

Metadata
Show full item record
Citation
Martin 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.
Publisher
Elsevier Ireland Ltd
Journal
Cancer letters
URI
http://hdl.handle.net/10147/323264
DOI
10.1016/j.canlet.2013.01.046
PubMed ID
23376256
Abstract
DNA 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.
Item Type
Article
Language
en
ISSN
1872-7980
Collections