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Updated: Sep 26, 2025

Silencing of BRCA2 to Identify Novel BRCA2-regulated Biological Functions in Cultured Human Cells
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Inhibition of APE1 Expression Enhances the Antitumor Activity of Olaparib in Triple-Negative Breast Cancer

Dan Jian1, Xue-Mei Li1, Nan Dai1

  • 1Cancer Center, Daping Hospital, Army Medical University, Chongqing 400042, China.

Evidence-Based Complementary and Alternative Medicine : Ecam
|April 25, 2022
PubMed

Insights

Targeting APE1 enhances PARP1 inhibitor efficacy in triple-negative breast cancer (TNBC). This study reveals APE1

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Therapeutics

Background:

  • Triple-negative breast cancer (TNBC) is aggressive with limited treatment options due to the absence of ER, PR, and HER2.
  • PARP1 inhibitors show promise but require optimization for TNBC treatment.

Purpose of the Study:

  • To investigate the molecular role of APE1 in PARP1-targeted therapy for TNBC.
  • To evaluate the effects of APE1 modulation on TNBC cell proliferation and apoptosis.

Main Methods:

  • Examined proliferation inhibition and apoptosis induction of PARP1 inhibitors in TNBC cells and xenograft models.
  • Assessed APE1 and PARP1 expression correlation in TNBC patients.
  • Investigated the impact of APE1 knockdown on olaparib sensitivity.

Main Results:

  • High APE1 and PARP1 expression in TNBC patients correlates with poor survival.
  • Knockdown of APE1 significantly increases sensitivity to the PARP1 inhibitor olaparib in TNBC.
  • APE1 plays a key role in the response to PARP1-targeted therapy.

Conclusions:

  • APE1 is a crucial molecular target in PARP1-inhibitor therapy for TNBC.
  • Targeting both APE1 and PARP1 offers a potential strategy for treating refractory TNBC.
  • This research provides a basis for future clinical applications in TNBC treatment.

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