Schisandrin A inhibits triple negative breast cancer cells by regulating Wnt/ER stress signaling pathway
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Updated: Jan 25, 2026

Studying Triple Negative Breast Cancer Using Orthotopic Breast Cancer Model
Published on: March 20, 2020
Xiaohong Xu1, Vinothakumar Rajamanicham1, Sujing Xu1
1Chemical Biology Research Center, School of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou, Zhejiang, 325035, PR China.
Abstract:
Triple-negative breast cancer (TNBC) is a subtype of breast cancer lacking prognostic and effective therapeutic targets currently. In this study, we evaluated the toxic potential of schisandrin A (SchA), a bioactive phytochemical found in Schisandra chinensis in TNBC. The anti-cancer effect and underlying mechanism of SchA on MDA-MB-231 and BT-549 cells were determined in vitro and in xenograft mouse model. Our data show that SchA markedly inhibited the growth of TNBC cells via induction of cell cycle arrest and cell apoptosis. Moreover, over activation of Wnt signaling was observed in TNBC cells, which was significantly suppressed by the treatment of SchA. Also, SchA treatment activated ER stress in TNBC cells. Finally, we verified these inhibitory effects of SchA in the MDA-MB-231 xenograft mouse model. In conclusion, SchA effectively inhibited TNBC in preclinical models by inducing cell cycle arrest and apoptosis via regulating Wnt/ER stress signaling pathway. All of these data indicate that SchA could be a potential candidate for the treatment of TNBC.
Insights
Schisandrin A (SchA) shows promise for treating triple-negative breast cancer (TNBC). This compound inhibits TNBC cell growth by inducing apoptosis and cell cycle arrest, offering a potential new therapeutic strategy.
Area of Science:
- Oncology
- Pharmacology
- Biochemistry
Background:
- Triple-negative breast cancer (TNBC) lacks effective therapeutic targets.
- Schisandrin A (SchA), a phytochemical from Schisandra chinensis, has potential anti-cancer properties.
Purpose of the Study:
- To evaluate the anti-cancer effects and mechanisms of SchA in TNBC.
- To investigate SchA's impact on Wnt signaling and ER stress in TNBC cells.
Main Methods:
- In vitro studies using MDA-MB-231 and BT-549 TNBC cell lines.
- In vivo evaluation in a xenograft mouse model.
- Analysis of cell cycle, apoptosis, Wnt signaling, and ER stress pathways.
Main Results:
- SchA significantly inhibited TNBC cell growth, inducing cell cycle arrest and apoptosis.
- SchA suppressed the overactivated Wnt signaling pathway in TNBC cells.
- SchA treatment activated ER stress in TNBC cells, confirmed in a xenograft model.
Conclusions:
- SchA demonstrates potent anti-cancer activity against TNBC in preclinical models.
- The mechanism involves inducing cell cycle arrest and apoptosis via regulation of Wnt/ER stress signaling.
- SchA represents a potential therapeutic candidate for TNBC treatment.
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