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Arctigenin Induces Mitochondrial Apoptosis in Ovarian Cancer Cells by Downregulating Bcl2L12 Expression

Ying Yang1,2, Peng Cui1, Weiyan Chen1

  • 1Key Laboratory of Ministry of Education for TCM Viscera-State Theory and Applications, Liaoning University of Traditional Chinese Medicine, Shenyang 110847, China.

Combinatorial Chemistry & High Throughput Screening
|June 19, 2026
PubMed
Abstract

Insights

Arctigenin induces apoptosis in ovarian cancer by targeting BCL2-like protein 12 (BCL2L12), a key factor in cancer cell survival. This study highlights arctigenin

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Ovarian cancer is a leading cause of gynecological cancer deaths due to late diagnosis and treatment resistance.
  • BCL2-like protein 12 (BCL2L12) plays an anti-apoptotic role, contributing to treatment challenges in ovarian cancer.
  • Understanding BCL2L12's function is crucial for developing novel therapeutic strategies against ovarian cancer.

Purpose of the Study:

  • To investigate the anti-apoptotic role of BCL2L12 in ovarian cancer.
  • To determine if arctigenin induces apoptosis by targeting BCL2L12 in ovarian cancer cells.
  • To evaluate the therapeutic potential of arctigenin as a BCL2L12 inhibitor.

Main Methods:

  • BCL2L12 knockdown and overexpression in SK-OV-3 and OVCAR-3 ovarian cancer cell lines.
  • Assays for cell viability, proliferation, apoptosis, mitochondrial membrane potential, and reactive oxygen species (ROS).
  • Western blotting for apoptosis- and autophagy-related proteins and analysis of public databases for BCL2L12 expression and prognosis.

Main Results:

  • BCL2L12 is upregulated in ovarian cancer, correlating with advanced stage and poor prognosis.
  • BCL2L12 silencing reduced cell growth, increased apoptosis, and inhibited autophagy.
  • Arctigenin inhibited proliferation, downregulated BCL2L12, and induced apoptosis; BCL2L12 overexpression counteracted these effects.

Conclusions:

  • BCL2L12 functions as an anti-apoptotic factor in ovarian cancer by preserving mitochondrial integrity.
  • Arctigenin effectively induces apoptosis by suppressing BCL2L12 and activating caspase-3/7.
  • Arctigenin demonstrates potential as a low-toxicity therapeutic agent for ovarian cancer by targeting BCL2L12.
Keywords:
BCL2L12OVCAR-3SK-OV-3apoptosisarctigenincaspase-3/7.mitochondrial pathway

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