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Apigenin modulates cell survival pathways and restores olaparib sensitivity in high-grade serous ovarian cancer cells

Jenn-Jhy Tseng1, Yeun-Ting Hsieh2, Chien-Hsing Lu3

  • 1Department of Obstetrics, Gynecology and Women's Health, Taichung Veterans General Hospital, Taichung, Taiwan; Department of Post-Baccalaureate Medicine, College of Medicine, National Chung Hsing University, Taichung, Taiwan; Department of Nursing, College of Nursing, HungKuang University, Taichung, Taiwan.

Taiwanese Journal of Obstetrics & Gynecology
|January 30, 2026
PubMed
Abstract

Insights

Apigenin (API) suppresses high-grade serous ovarian cancer (HGSOC) progression and restores sensitivity to poly (ADP-ribose) polymerase inhibitors (PARPi) like olaparib in resistant cells. This flavonoid modulates survival pathways, induces apoptosis, and arrests the cell cycle, showing promise as an adjuvant therapy.

Area of Science:

  • Oncology
  • Molecular Biology
  • Pharmacology

Background:

  • High-grade serous ovarian cancer (HGSOC) is challenging due to resistance to therapies like poly (ADP-ribose) polymerase inhibitors (PARPi).
  • Apigenin (API), a natural flavonoid, has potential therapeutic properties.
  • Investigating API's role in overcoming PARPi resistance in HGSOC is crucial.

Purpose of the Study:

  • To investigate apigenin's (API) potential to modulate survival pathways in HGSOC.
  • To determine if API can restore sensitivity to olaparib in HGSOC cell lines.
  • To explore API's effects on cell viability, apoptosis, and cell cycle progression.

Main Methods:

  • Utilized four human HGSOC cell lines and their olaparib-resistant derivatives.
  • Assessed cell viability, apoptosis, and cell cycle distribution via MTT assays and flow cytometry.
  • Analyzed key protein phosphorylation (STAT3, AKT), apoptotic markers, and cell cycle regulators using Western blotting and immunofluorescence.

Main Results:

  • Apigenin (API) reduced cell viability and induced apoptosis or cell cycle arrest (G2/M phase) in HGSOC cell lines.
  • API selectively inhibited phosphorylated STAT3 (pSTAT3) and AKT (pAKT), key survival pathway components.
  • API restored olaparib sensitivity in resistant cells, linked to reduced pSTAT3 levels, suggesting STAT3 modulation as a resistance-reversal mechanism.

Conclusions:

  • Apigenin (API) effectively suppresses HGSOC progression through apoptosis induction and cell cycle arrest.
  • API modulates critical survival pathways, including STAT3 and AKT signaling.
  • API demonstrates potential as an adjuvant therapy to enhance olaparib efficacy in overcoming PARPi resistance in HGSOC.
Keywords:
ApigeninHigh-grade serous ovarian cancer (HGSOC)Olaparib resistancePARP inhibitorSTAT3 signaling

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