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.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 19-25 |
| Number of pages | 7 |
| Journal | Cancer Letters |
| Volume | 335 |
| Issue number | 1 |
| DOIs | |
| State | Published - Jul 10 2013 |
| Externally published | Yes |
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Keywords
- Cell cycle arrest
- DNA mismatch repair
- Endometrial
- G2/M
- Hypersensitivity
- Ionizing radiation
- Low dose
- MSH2
ASJC Scopus subject areas
- Oncology
- Cancer Research
Cite this
DNA mismatch repair protein MSH2 dictates cellular survival in response to low dose radiation in endometrial carcinoma cells. / Martin, Lynn M.; Marples, Brian; Davies, Anthony M.; Atzberger, Ann; Edwards, Connla; Lynch, Thomas H.; Hollywood, Donal; Marignol, Laure.
In: Cancer Letters, Vol. 335, No. 1, 10.07.2013, p. 19-25.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - DNA mismatch repair protein MSH2 dictates cellular survival in response to low dose radiation in endometrial carcinoma cells
AU - Martin, Lynn M.
AU - Marples, Brian
AU - Davies, Anthony M.
AU - Atzberger, Ann
AU - Edwards, Connla
AU - Lynch, Thomas H.
AU - Hollywood, Donal
AU - Marignol, Laure
PY - 2013/7/10
Y1 - 2013/7/10
N2 - 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.
AB - 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.
KW - Cell cycle arrest
KW - DNA mismatch repair
KW - Endometrial
KW - G2/M
KW - Hypersensitivity
KW - Ionizing radiation
KW - Low dose
KW - MSH2
UR - http://www.scopus.com/inward/record.url?scp=84878427186&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84878427186&partnerID=8YFLogxK
U2 - 10.1016/j.canlet.2013.01.046
DO - 10.1016/j.canlet.2013.01.046
M3 - Article
C2 - 23376256
AN - SCOPUS:84878427186
VL - 335
SP - 19
EP - 25
JO - Cancer Letters
JF - Cancer Letters
SN - 0304-3835
IS - 1
ER -