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Unveiling tectorigenin: A novel ferroptosis inducer targeting EGFR in bladder cancer
Jiancheng Zhai1, Rong Tan2, Shenglan Yuan3
1Department of Urology & Andrology, The First Affiliated Hospital of Guizhou University of Traditional Chinese Medicine, No. 71 Bao Shan North Road, Yunyan District, Guiyang 550001, Guizhou, China; School of Pharmacy, Zhejiang Chinese Medical University 310053, Hangzhou, China.
Background:
Bladder cancer is a frequently occurring urinary tumour with significant incidence and mortality rates. Tectorigenin, extracted from Belamcanda chinensis (L.) Redouté, possesses several biomedical activities, including anticancer properties.
Purpose:
To investigate the effectiveness and mechanism of tectorigenin in bladder cancer.
Methods:
Tectorigenin's effects and mechanisms were investigated using the Cell Counting Kit-8 (CCK8) test, fluorescence detection, flow cytometry, transmission electron microscopy (TEM), Western blotting, ferroptosis analysis, molecular dynamics simulations, and molecular docking. Tectorigenin's effects were also evaluated in the 5637 cell xenograft model.
Results:
Tectorigenin significantly inhibited tumour growth and decreased Ki67 levels with no significant organ damage and toxicity. And the anti-tumour effects of tectorigenin (100 mg/kg) were similar to those of the cisplatin (3 mg/kg) group. In vitro experiments indicated that tectorigenin inhibited cell proliferation, increased reactive oxygen species (ROS), induced apoptosis, and decreased mitochondrial membrane potential (MMP) in T24 and 5637 cell lines. Moreover, tectorigenin induced ferroptosis, as demonstrated by mitochondrial damage detected via TEM, increased Fe²⁺ concentrations, and reduced levels of solute carrier family 7 member 11 (xCT), glutathione peroxidase 4 (GPX4), and glutathione (GSH). All ferroptosis effects elicited by tectorigenin were attenuated by deferoxamine (DFO). The epidermal growth factor receptor (EGFR) was recognised as a crucial target, with tectorigenin demonstrating a notable binding affinity of -8.0 kcal/mol. Additionally, the ferroptotic effects, induction of apoptosis, increase in ROS, and decrease in MMP of tectorigenin on 5637 cells were reversed by EGF pretreatment. Moreover, tectorigenin suppressed tumour growth in bladder cancer, and its anticancer effect was partially diminished by DFO.
Conclusion:
This study is the first to propose that tectorigenin functions as a novel agent that induces ferroptosis in bladder cancer by targeting EGFR. Our findings reveal a novel therapeutic mechanism and lay the groundwork for developing targeted treatments for bladder cancer.
Insights
Tectorigenin, a natural compound, effectively inhibits bladder cancer growth by inducing ferroptosis, a form of cell death, through targeting the epidermal growth factor receptor (EGFR). This discovery offers a new therapeutic strategy for bladder cancer treatment.
Area of Science:
- Oncology
- Pharmacology
- Biochemistry
Background:
- Bladder cancer presents significant global health challenges due to high incidence and mortality.
- Tectorigenin, derived from Belamcanda chinensis, exhibits promising anticancer properties.
Purpose of the Study:
- To elucidate the efficacy and underlying mechanisms of tectorigenin in combating bladder cancer.
- To explore tectorigenin's potential as a novel therapeutic agent for bladder cancer.
Main Methods:
- In vitro assays (CCK8, fluorescence, flow cytometry, TEM) and in vivo xenograft models were employed.
- Western blotting, ferroptosis analysis, molecular dynamics, and docking studies investigated mechanisms.
- Key molecular targets and signaling pathways were analyzed.
Main Results:
- Tectorigenin significantly suppressed bladder tumor growth in vivo, comparable to cisplatin, with no observed organ toxicity.
- In vitro, tectorigenin inhibited proliferation, induced apoptosis, increased reactive oxygen species (ROS), and decreased mitochondrial membrane potential (MMP).
- Tectorigenin triggered ferroptosis by damaging mitochondria, increasing Fe²⁺, and reducing xCT, GPX4, and GSH levels, with effects reversed by deferoxamine (DFO) and epidermal growth factor (EGF).
Conclusions:
- Tectorigenin acts as a novel ferroptosis-inducing agent in bladder cancer, specifically by targeting the epidermal growth factor receptor (EGFR).
- This study reveals a new therapeutic mechanism for tectorigenin, paving the way for targeted bladder cancer therapies.
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