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Oxidative DNA Damage-Mediated Genomic Heterogeneity Is Regulated by NKX3.1 in Prostate Cancer

Bilge Debelec-Butuner1, Aykut Bostancı2, Filiz Ozcan3

  • 1a Department of Pharmaceutical Biotechnology, Faculty of Pharmacy , Ege University , Izmir , Turkey.

Cancer Investigation
|March 7, 2019
PubMed

Insights

NKX3.1 plays a crucial role in repairing oxidative DNA damage, specifically 8-hydroxy-2'-deoxyguanosine (8-OHdG) formation. Its overexpression aids in removing this damage, correlating with OGG1 expression.

Area of Science:

  • Molecular Biology
  • Oxidative Stress Research
  • Genetics

Background:

  • 8-hydroxy-2 -deoxyguanosine (8-OHdG) is a key marker of DNA damage caused by reactive oxygen species.
  • The roles of Androgen Receptor and NKX3.1 in oxidative DNA damage and repair remain incompletely understood.

Purpose of the Study:

  • To investigate the involvement of Androgen Receptor and NKX3.1 in the formation and repair of 8-OHdG.
  • To establish and utilize a novel cell-based method for quantifying 8-OHdG DNA damage.

Main Methods:

  • Quantitation of 8-OHdG DNA damage using the Aklides.NUK system.
  • Analysis of NKX3.1 and 8-oxoguanine DNA glycosylase-1 (OGG1) expression levels.
  • Investigating the effects of NKX3.1 loss and overexpression on oxidative DNA damage.

Main Results:

  • Loss of NKX3.1 significantly increased oxidative DNA damage (8-OHdG).
  • Overexpression of NKX3.1 facilitated the removal of menadione-induced 8-OHdG, even under oxidative stress.
  • NKX3.1 expression positively correlated with OGG1 expression levels.

Conclusions:

  • NKX3.1 is a critical regulator in the cellular response to oxidative DNA damage.
  • NKX3.1's role in 8-OHdG repair is linked to OGG1 expression.
  • A reliable cell-based method for 8-OHdG quantitation has been developed and validated.
Keywords:
8-OHdGAklidesAndrogen receptorNKX3.1

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