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Triumphs and challenges in exploiting poly(ADP-ribose) polymerase inhibition to combat triple-negative breast cancer

Jonathan Wooten1,2, Nicole Mavingire1, Katherine Damar1

  • 1Department of Basic Sciences, Division of Pharmacology, School of Medicine, Loma Linda University Health, Loma Linda, California, USA.

Journal of Cellular Physiology
|April 12, 2023
PubMed

Insights

Poly(ADP-ribose) polymerase inhibitors (PARPi) target DNA repair in homologous recombination-deficient cancers like triple-negative breast cancer (TNBC). This review explores PARP

Area of Science:

  • Oncology
  • Genetics
  • Molecular Biology

Background:

  • Poly(ADP-ribose) polymerase 1 (PARP1) is crucial for DNA repair, maintaining genomic stability.
  • PARP inhibitors (PARPi) leverage synthetic lethality in homologous recombination (HR) deficient cancers.
  • Triple-negative breast cancer (TNBC) often lacks targeted therapy options due to specific receptor deficiencies.

Purpose of the Study:

  • To review the role of PARP in DNA repair within breast epithelial cells.
  • To elucidate mechanisms of PARP inhibitor resistance in TNBC.
  • To discuss emerging strategies to overcome PARP inhibitor resistance in TNBC.

Main Methods:

  • Literature review of PARP function in DNA repair.
  • Analysis of mechanisms underlying PARPi resistance in TNBC.
  • Survey of novel therapeutic agents targeting PARPi resistance.

Main Results:

  • PARP1 plays a significant role in DNA damage response pathways.
  • Mutations in HR genes (e.g., BRCA1/2) sensitize TNBC to PARPi.
  • De novo and acquired resistance to PARPi is a significant clinical challenge in TNBC.

Conclusions:

  • Understanding PARP's role in DNA repair is key to TNBC treatment.
  • Mechanisms of PARPi resistance require further investigation.
  • Development of novel agents is critical to improve outcomes for TNBC patients resistant to PARPi.
Keywords:
DNA damage repairPARP inhibitor resistancepoly(ADP)-ribose polymerase (PARP)synthetic lethalitytriple-negative breast cancer

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