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Manipulating PARK7/DJ-1 Levels by Genotoxic Stress Alters Noncoding RNAs and Cellular Homeostasis.

Keren Zohar1, Haya Zoubi2, Michal Goldberg2

  • 1Department of Biological Chemistry, Institute of Life Sciences, The Hebrew University of Jerusalem, Jerusalem 9190401, Israel.

Cells
|December 10, 2025
PubMed
Summary

The protein DJ-1 (also known as PARK7) significantly alters cellular responses to DNA damage. Its manipulation impacts gene expression, stress pathways, and non-coding RNAs, highlighting its role in cancer and oxidative stress.

Keywords:
Parkinson’s diseaseRNA-seqX-raylncRNAmiRNAsoxidation stressregulated cell deathribosome stabilitysiRNA

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Area of Science:

  • Molecular Biology
  • Genetics
  • Cell Biology

Background:

  • DJ-1/PARK7 is a key protein in sensing oxidative stress and maintaining redox balance.
  • As an oncogene, DJ-1 affects p53-mediated stress responses and cancer progression.
  • Understanding DJ-1's role in DNA damage response is crucial for disease therapeutics.

Purpose of the Study:

  • To investigate how X-ray-induced DNA breaks affect cellular responses based on DJ-1 expression levels.
  • To analyze transcriptional changes under varying DJ-1 expression following DNA damage.
  • To explore the impact of DJ-1 on non-coding RNA profiles during genotoxic stress.

Main Methods:

  • Utilized siRNA knockdown and overexpression to manipulate DJ-1 levels.
  • Employed RNA sequencing (RNA-seq) to analyze global transcriptional changes.
  • Assessed cellular responses to X-ray irradiation.

Main Results:

  • DJ-1 overexpression suppressed ribosomal and mitochondrial gene expression significantly after X-ray exposure.
  • DJ-1 knockdown disrupted cellular homeostasis, causing widespread transcriptional changes.
  • DJ-1 manipulation altered non-coding RNA expression, including lncRNAs and snoRNAs.
  • DJ-1 knockdown cells showed suppressed DNA-damage response genes upon irradiation.

Conclusions:

  • DJ-1 critically modulates cellular responses to genotoxic stress by reshaping transcriptional landscapes.
  • DJ-1's influence on redox and transcriptional networks suggests its potential as a therapeutic target.
  • Altered ncRNA profiles and ribosomal regulation by DJ-1 have implications for disease pathogenesis.