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Eupalinolide O Induces Apoptosis in Human Triple-Negative Breast Cancer Cells via Modulating ROS Generation and
Yaping Zhao1, Liping Fu1, Jinbai Chen1
1Department of Pharmacy, Shaoxing Hospital of Traditional Chinese Medicine Affiliated to Zhejiang Chinese Medical University, Shaoxing, Zhejiang 312000, China.
Background:
Triple-negative breast cancer (TNBC) is a subtype of breast cancer with limited therapeutic options. Eupalinolide O (EO) was reported to inhibit tumor growth. This study is aimed at exploring the role of EO on TNBC both in vivo and in vitro. Methods. In in vitro experiments, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) and clonogenic assay were conducted to measure the impact of EO on TNBC cell growth at different concentrations and time points. Flow cytometry was conducted to evaluate cell apoptosis. Mitochondrial membrane potential (MMP) loss, caspase-3 activity, and reactive oxygen species (ROS) generation were assessed. The expressions of apoptosis-related mRNAs and Akt/p38 MAPK signaling pathway-related proteins were measured. In in vivo experiments, by injecting TNBC cells into the nude mice to induce xenograft tumor, mice were treated with EO for 20 days. Then, in vivo bioluminescence imaging system was utilized to monitor the growth and distribution of TNBC cells. Tumor volume and weight were also recorded. Hematoxylin-eosin (HE) staining and ELISA assay were applied to observe tumor tissue morphology and ROS levels. Furthermore, western blotting was conducted to observe the expression of apoptosis-related proteins and Akt/p38 MAPK signaling pathway-associated proteins.
Results:
EO inhibited the cell viability and proliferation of TNBC cells but not normal epithelial cells. Furthermore, EO induced apoptosis, decreased MMP, and elevated caspase-3 activity and ROS content in TNBC cells. Meanwhile, the expression of apoptosis-related mRNAs and Akt/p38 MAPK pathway-related proteins was regulated by EO treatment. Besides, in vivo experiments demonstrated EO not only suppressed tumor growth, Ki67 expression, ROS generation, and Akt phosphorylation but also upregulated caspase-3 expression and p-38 phosphorylation.
Conclusion:
EO may induce cell apoptosis in TNBC via regulating ROS generation and Akt/p38 MAPK pathway, indicating EO may be a candidate drug for TNBC.
Insights
Eupalinolide O (EO) effectively inhibits triple-negative breast cancer (TNBC) cell growth and proliferation by inducing apoptosis. This study suggests EO is a potential therapeutic candidate for TNBC treatment.
Area of Science:
- Biochemistry
- Molecular Biology
- Oncology
Background:
- Triple-negative breast cancer (TNBC) presents limited therapeutic options.
- Eupalinolide O (EO) has demonstrated tumor growth inhibitory effects.
- This study investigates the efficacy of EO against TNBC.
Purpose of the Study:
- To explore the anti-cancer effects of Eupalinolide O (EO) on triple-negative breast cancer (TNBC) both in vitro and in vivo.
- To elucidate the molecular mechanisms underlying EO's action on TNBC cells.
- To evaluate EO as a potential therapeutic agent for TNBC.
Main Methods:
- In vitro: MTT and clonogenic assays for cell viability/proliferation, flow cytometry for apoptosis, assessment of mitochondrial membrane potential (MMP), caspase-3 activity, and reactive oxygen species (ROS). Gene and protein expression analysis of apoptosis-related factors and Akt/p38 MAPK pathway.
- In vivo: TNBC xenograft mouse models, bioluminescence imaging, tumor volume/weight measurement, HE staining, ELISA for ROS, and Western blotting for protein expression.
Main Results:
- EO inhibited TNBC cell viability and proliferation without affecting normal cells.
- EO induced apoptosis, decreased MMP, and increased caspase-3 activity and ROS in TNBC cells.
- EO suppressed tumor growth, Ki67, ROS generation, and Akt phosphorylation, while upregulating caspase-3 and p-38 phosphorylation in vivo.
Conclusions:
- Eupalinolide O (EO) induces apoptosis in triple-negative breast cancer (TNBC) by modulating ROS generation and the Akt/p38 MAPK pathway.
- EO demonstrates potential as a therapeutic candidate for TNBC treatment.
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