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

Lynn M. Martin; Brian Marples; Anthony M. Davies; Ann Atzberger; Connla Edwards; Thomas H. Lynch; Donal Hollywood; Laure Marignol

doi:10.1016/j.canlet.2013.01.046

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

Lynn M. Martin, Brian Marples, Anthony M. Davies, Ann Atzberger, Connla Edwards, Thomas H. Lynch, Donal Hollywood, Laure Marignol

Research output: Contribution to journal › Article › peer-review

11 Scopus citations

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	https://doi.org/10.1016/j.canlet.2013.01.046
State	Published - Jul 10 2013
Externally published	Yes

Keywords

Cell cycle arrest
DNA mismatch repair
Endometrial
G2/M
Hypersensitivity
Ionizing radiation
Low dose
MSH2

ASJC Scopus subject areas

Oncology
Cancer Research

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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 › peer-review

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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.",

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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

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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

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KW - Low dose

KW - MSH2

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

Abstract

Keywords

ASJC Scopus subject areas

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