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MYC inhibition by Omomyc causes DNA damage and overcomes PARPi resistance in breast cancer

Fabio Giuntini1, Íñigo González-Larreategui1, Andrea Herencia-Ropero2

  • 1Models of Cancer Therapies Group, Vall d'Hebron Institute of Oncology (VHIO), Vall d'Hebron Barcelona Hospital Campus, Barcelona, Spain.

Cell Reports
|November 22, 2025
PubMed

Insights

Omomyc, a MYC inhibitor, disrupts DNA repair in triple-negative breast cancer (TNBC). Combining Omomyc with PARP inhibitors shows promise for treating PARP inhibitor-resistant TNBC.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Genetics

Background:

  • MYC dysregulation is common in cancers, influencing DNA damage response (DDR).
  • MYC acts as a dual modulator of genomic instability and DNA repair.
  • Triple-negative breast cancer (TNBC) presents therapeutic challenges.

Purpose of the Study:

  • To investigate the effect of Omomyc, a direct MYC inhibitor, on DDR in TNBC.
  • To evaluate the efficacy of combining Omomyc with poly ADP-ribose polymerase inhibitors (PARPis) in TNBC models.
  • To identify MYC's role as a potential biomarker for PARPi resistance.

Main Methods:

  • Treatment of TNBC models with Omomyc and/or PARPis.
  • Assessment of DDR gene expression, DNA damage induction, and cell viability.
  • In vitro and in vivo studies using patient-derived models and clinical samples.

Main Results:

  • Omomyc inhibits DDR genes in TNBC, leading to DDR defects and DNA damage.
  • Omomyc enhances PARPi-induced DNA damage and exhibits synergistic effects with PARPis.
  • Combination therapy overcomes both intrinsic and acquired PARPi resistance.
  • MYC activity predicts PARPi resistance in patient-derived TNBC models.

Conclusions:

  • Omomyc combined with PARPis offers a potential therapeutic strategy for PARPi-resistant TNBC.
  • MYC transcriptional activity serves as a predictive biomarker for PARPi resistance in TNBC.
  • This combination approach warrants further clinical investigation for TNBC treatment.
Keywords:
CP: cancerDNA damageOmomycPARPiTNBCtherapy resistance

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