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Ubiquitin's code: UPS orchestrating DNA repair and genomic stability under genotoxic stress

Srija Roy1, Gouranga Saha1, Malini Basu2

  • 1Cancer Biology and Inflammatory Disorder Division, TRUE Campus, Council of Scientific and Industrial Research-Indian Institute of Chemical Biology (CSIR-IICB), CN-6, Sector-V, Salt Lake, Kolkata, 700091, India.

Molecular and Cellular Biochemistry
|May 12, 2026
PubMed

Insights

DNA damage from various agents can cause genomic instability and cancer. E3 ubiquitin ligases and deubiquitinases (DUBs) regulate DNA repair, offering potential targets for overcoming cancer chemoresistance.

Area of Science:

  • Genetics
  • Molecular Biology
  • Oncology

Background:

  • DNA damage from physical and chemical agents is a major cause of genomic instability and cancer.
  • Agents like radiation, chemotherapy, and redox imbalance induce DNA lesions, compromising genomic integrity.
  • E3 ubiquitin ligases and deubiquitinases (DUBs) are critical regulators of DNA damage tolerance and repair pathways.

Purpose of the Study:

  • To review the role of ubiquitination and deubiquitination in DNA damage repair.
  • To highlight the involvement of E3 ubiquitin ligases and DUBs in maintaining genomic integrity.
  • To explore the potential of targeting these ubiquitination processes to combat cancer chemoresistance.

Main Methods:

  • Literature review focusing on ubiquitination, deubiquitination, and DNA repair.
  • Analysis of the interplay between E3 ubiquitin ligases, DUBs, and DNA damage response pathways.
  • Synthesis of current understanding regarding the impact of these processes on cancer chemoresistance.

Main Results:

  • Ubiquitination and deubiquitination dynamically control DNA damage tolerance and repair.
  • Dysregulation of E3 ubiquitin ligases and DUBs can lead to increased chemoresistance by upregulating DNA repair proteins.
  • These enzymes represent critical nodes in safeguarding genomic integrity against various DNA damaging agents.

Conclusions:

  • The coordinated action of E3 ubiquitin ligases and DUBs is essential for effective DNA repair and genomic stability.
  • Targeting ubiquitination and deubiquitination pathways presents a promising strategy for enhancing cancer therapy efficacy.
  • Understanding these intricate molecular mechanisms is key to developing novel approaches to overcome cancer chemoresistance.
Keywords:
CancerDNA damage repairGenomic instabilityGenotoxic stressUbiquitin signalling

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