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Updated: Sep 18, 2025
Studying Triple Negative Breast Cancer Using Orthotopic Breast Cancer Model
Published on: March 20, 2020
Multi-Targeted Anti-Cancer Effects of Triptophenolide in Hormone-Responsive and Triple-Negative Breast Cancer Models
Zufa Sabeel1, Guangshuai Chai1, Ruolan Chen1
1State Key Laboratory of Green Biomanufacturing, College of Life Science and Technology, Innovation Center of Molecular Diagnostics, Beijing University of Chemical Technology, Beijing 100029, China.
Abstract:
Breast cancer (BC) remains a significant therapeutic challenge, necessitating novel agents with multi-target efficacy. Here, we demonstrate that triptophenolide (TRI), a bioactive compound from Tripterygium wilfordii, exerts potent anti-BC activity across hormone-responsive (MCF-7) and triple-negative (MDA-MB-231) subtypes. In vitro, TRI inhibited proliferation in a concentration-dependent manner, with IC50 values decreasing from 180.3 μg/mL (24 h) to 127.2 μg/mL (48 h) in MCF-7 cells, and from 322.5 μg/mL to 262.1 μg/mL in MDA-MB-231 cells. TRI treatment induced G1-phase arrest in both breast cancer subtypes, increasing the G1 population by 22.27% in MCF-7 cells and 10.64% in MDA-MB-231 cells. Concurrently, TRI triggered apoptosis, elevating apoptotic rates from 3.36% to 9.78% in MCF-7 cells and from 7.01% to 17.02% in MDA-MB-231 cells. These effects were associated with the significant upregulation of pro-apoptotic proteins BAX, BAK1, BIM, and cytochrome c (CYCS). Notably, TRI suppressed migration by 61.5% (MCF-7) and 71.5% (MDA-MB-231). In vivo, TRI treatment inhibited MCF-7 xenograft growth and reduced tumor volume (1207.5 vs. 285 mm3) and weight (0.22 vs. 0.1 g), while extending the survival time of tumor-bearing mice from 14-20 days to 24 days. These results position TRI as a promising lead therapeutic candidate against diverse BC subtypes, with mechanistic versatility surpassing single-target agents.
Insights
Triptophenolide (TRI) shows strong anti-breast cancer effects against multiple subtypes by inhibiting growth and promoting apoptosis. This natural compound also reduced tumor size and improved survival in preclinical models, offering a versatile therapeutic option.
Area of Science:
- Pharmacology and Toxicology
- Molecular Biology
- Oncology
Background:
- Breast cancer (BC) presents a significant therapeutic challenge, requiring novel agents with multi-target efficacy.
- Existing treatments often lack broad efficacy across diverse BC subtypes, including hormone-responsive and triple-negative forms.
Purpose of the Study:
- To investigate the anti-cancer potential of triptophenolide (TRI), a compound derived from Tripterygium wilfordii, against various breast cancer subtypes.
- To elucidate the mechanisms underlying TRI's efficacy, including its effects on cell proliferation, cell cycle progression, apoptosis, and migration.
Main Methods:
- In vitro studies using MCF-7 (hormone-responsive) and MDA-MB-231 (triple-negative) breast cancer cell lines.
- Assessment of cell proliferation, cell cycle distribution (G1-phase arrest), apoptosis induction, and cell migration.
- Analysis of key pro-apoptotic protein expression (BAX, BAK1, BIM, cytochrome c).
- In vivo efficacy evaluation using MCF-7 xenograft models in mice.
Main Results:
- TRI significantly inhibited proliferation and induced G1-phase cell cycle arrest in both BC subtypes.
- TRI treatment markedly increased apoptosis rates and upregulated pro-apoptotic proteins (BAX, BAK1, BIM, CYCS).
- TRI suppressed cancer cell migration and demonstrated significant tumor growth inhibition, reduced tumor volume/weight, and extended survival in vivo.
Conclusions:
- Triptophenolide (TRI) exhibits potent, multi-targeted anti-breast cancer activity against both hormone-responsive and triple-negative subtypes.
- TRI's mechanisms involve cell cycle arrest, apoptosis induction, and suppressed migration, positioning it as a promising therapeutic lead.
- The findings support TRI's potential as a versatile agent for diverse breast cancer treatment strategies.
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