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 journalArticle

10 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 languageEnglish (US)
Pages (from-to)19-25
Number of pages7
JournalCancer letters
Volume335
Issue number1
DOIs
StatePublished - Jul 10 2013
Externally publishedYes

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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