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Human AP endonuclease 1 (APE1): from mechanistic insights to druggable target in cancer

Rachel Abbotts1, Srinivasan Madhusudan

  • 1Translational DNA Repair Group, Laboratory of Molecular Oncology, Academic Unit of Oncology, School of Molecular Medical Sciences, University of Nottingham, Nottingham, UK.

Cancer Treatment Reviews
|January 9, 2010
PubMed

Insights

Human apurinic/apyrimidinic endonuclease 1 (APE1) is vital for DNA repair and a promising anticancer target. Inhibiting APE1 enhances chemotherapy effectiveness, showing potential for cancer treatment.

Area of Science:

  • Molecular Biology
  • Oncology
  • Biochemistry

Background:

  • DNA base excision repair (BER) processes DNA damage from alkylating agents.
  • PARP inhibitors show promise in clinical trials for cancer therapy.
  • Human apurinic/apyrimidinic endonuclease 1 (APE1) is crucial for BER pathway.
  • APE1 processes cytotoxic abasic sites, essential intermediates in BER.

Purpose of the Study:

  • Summarize the mechanistic role of APE1 in DNA repair and redox regulation.
  • Highlight preclinical and clinical data supporting APE1 as an anticancer drug target.
  • Discuss the development of small molecule inhibitors targeting APE1.

Main Methods:

  • Review of mechanistic role of APE1 in DNA repair and redox regulation.
  • Analysis of preclinical and clinical data on APE1 as a drug target.
  • Summary of research on small molecule inhibitors of APE1.

Main Results:

  • APE1 plays a fundamental role in DNA base excision repair.
  • APE1 is involved in redox regulation.
  • Preclinical and clinical data validate APE1 as a viable anticancer target.
  • APE1 inhibitors potentiate the cytotoxicity of alkylating agents in preclinical models.

Conclusions:

  • APE1 is a validated anticancer drug target.
  • Small molecule inhibitors of APE1 show translational applications in cancer therapy.
  • Inhibiting APE1 enhances the efficacy of alkylating agents.

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