Nkx3.1 controls the DNA repair response in the mouse prostate.

Autor: Zhang H; Department of Medicine and Pathology, Columbia University Medical Center, Herbert Irving Comprehensive Cancer Center, Columbia University, New York City, New York., Zheng T; Department of Medicine and Pathology, Columbia University Medical Center, Herbert Irving Comprehensive Cancer Center, Columbia University, New York City, New York.; Department of Statistics, Columbia University Medical Center, Herbert Irving Comprehensive Cancer Center, Columbia University, New York City, New York., Chua CW; Department of Medicine and Pathology, Columbia University Medical Center, Herbert Irving Comprehensive Cancer Center, Columbia University, New York City, New York.; Department of Developmental and Cell Biology, Columbia University Medical Center, Herbert Irving Comprehensive Cancer Center, Columbia University, New York City, New York., Shen M; Department of Medicine and Pathology, Columbia University Medical Center, Herbert Irving Comprehensive Cancer Center, Columbia University, New York City, New York.; Department of Developmental and Cell Biology, Columbia University Medical Center, Herbert Irving Comprehensive Cancer Center, Columbia University, New York City, New York., Gelmann EP; Department of Medicine and Pathology, Columbia University Medical Center, Herbert Irving Comprehensive Cancer Center, Columbia University, New York City, New York.
Jazyk: angličtina
Zdroj: The Prostate [Prostate] 2016 Mar; Vol. 76 (4), pp. 402-8. Date of Electronic Publication: 2015 Dec 10.
DOI: 10.1002/pros.23131
Abstrakt: Background: The human prostate tumor suppressor NKX3.1 mediates the DNA repair response and interacts with the androgen receptor to assure faithful completion of transcription thereby protecting against TMPRSS2-ERG gene fusion. To determine directly the effect of Nkx3.1 in vivo we studied the DNA repair response in prostates of mice with targeted deletion of Nkx3.1.
Methods: Using both drug-induced DNA damage and γ-irradiation, we assayed expression of γ-histone 2AX at time points up to 24 hr after induction of DNA damage.
Results: We demonstrated that expression of Nkx3.1 influenced both the timing and magnitude of the DNA damage response in the prostate.
Conclusions: Nkx3.1 affects the DNA damage response in the murine prostate and is haploinsufficient for this phenotype.
(© 2015 The Authors. The Prostate published by Wiley Periodicals, Inc.)
Databáze: MEDLINE
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