Fuzheng Yiai Formula and its Key Components Inhibited PCa by TP53/SLC7A11/GPX4-Induced Ferroptosis
5 affiliations
- 1School of Traditional Chinese Medicine, Hunan University of Medicine, No. 492 Jinxi South Road, Huaihua, 418000 China
- 2Medical School, Hunan University of Chinese Medicine, Changsha, 410208 China
- 3Andrology Laboratory, Hunan University of Chinese Medicine, Changsha, 410208 China
- 4School of Integrated Chinese and Western Medicine, Hunan University of Chinese Medicine, Changsha, 410208 China
- 5Hunan Chunguang Jiuhui Modern Chinese Medicine Co., Ltd., Liuyang, 410300 China
Abstract
Fuzheng Yiai Formula (FZYAF) is a traditional Chinese medicine compound, and its key components, ursolic acid (UA) and Anhydroicaritin (AHI), have potential antitumor activity, but their mechanisms of action in Prostate cancer (PCa) remain unclear.
Key components and targets of FZYAF were identified by network pharmacology, and the components were further validated by HPLC-MS analysis. PCa cells were treated with UA and AHI to assess their effects on cell proliferation, migration, and ferroptosis. The interaction of UA or AHI with TP53 was assessed by molecular docking and DARTS. In vivo, a PCa mouse model was established, and tumor tissues from FZYAF-treated mice were subjected to metabolomic analysis. Additionally, the anti-tumor effects of FZYAF, UA, and AHI, and their impact on ferroptosis and the TP53 pathway were evaluated.
Network pharmacology and HPLC-MS analysis, UA and AHI were identified as the key active components of FZYAF, and TP53 was predicted as a core target. In vitro, UA and AHI inhibited PCa cell proliferation and migration and induced ferroptosis, with their combination showing enhanced efficacy compared to either agent alone. Mechanistically, UA and AHI were bound to and upregulated the TP53 protein. In vivo, FZYAF inhibited tumor growth and induced ferroptosis in PCa mice, which was associated with alterations in lipid metabolism-related pathways, as revealed.
UA and AHI, key components of FZYAF, inhibit PCa progression by binding to and upregulating the TP53 protein to induce ferroptosis. This study elucidates the role of FZYAF in developing anti-PCa drugs.
Supplementary Information: The online version contains supplementary material available at https://doi.org/10.1186/s12575-026-00357-x.
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BibTeX
@article{sheng2026fuzheng,
title = {{Fuzheng Yiai Formula and its Key Components Inhibited PCa by TP53/SLC7A11/GPX4-Induced Ferroptosis}},
author = {Wen Sheng and Yingqiu Li and Xiaopeng Yu and Xiaoke Zeng and Yujie Jiang and Qingting Wu and Fanshun Shen and Xiye Ouyang and Qinghu He},
journal = {Biological Procedures Online},
year = {2026},
month = aug,
doi = {10.1186/s12575-026-00357-x},
url = {https://doi.org/10.1186/s12575-026-00357-x},
note = {CC BY-NC-ND 4.0},
}
RIS
TY - JOUR
TI - Fuzheng Yiai Formula and its Key Components Inhibited PCa by TP53/SLC7A11/GPX4-Induced Ferroptosis
AU - Wen Sheng
AU - Yingqiu Li
AU - Xiaopeng Yu
AU - Xiaoke Zeng
AU - Yujie Jiang
AU - Qingting Wu
AU - Fanshun Shen
AU - Xiye Ouyang
AU - Qinghu He
PY - 2026
DA - 2026/08/06
JO - Biological Procedures Online
DO - 10.1186/s12575-026-00357-x
UR - https://doi.org/10.1186/s12575-026-00357-x
AB - Fuzheng Yiai Formula (FZYAF) is a traditional Chinese medicine compound, and its key components, ursolic acid (UA) and Anhydroicaritin (AHI), have potential antitumor activity, but their mechanisms of action in Prostate cancer (PCa) remain unclear. Key components and targets of FZYAF were identified by network pharmacology, and the components were further validated by HPLC-MS analysis. PCa cells were treated with UA and AHI to assess their effects on cell proliferation, migration, and ferroptosis. The interaction of UA or AHI with TP53 was assessed by molecular docking and DARTS. In vivo, a PCa mouse model was established, and tumor tissues from FZYAF-treated mice were subjected to metabolomic analysis. Additionally, the anti-tumor effects of FZYAF, UA, and AHI, and their impact on ferroptosis and the TP53 pathway were evaluated. Network pharmacology and HPLC-MS analysis, UA and AHI were identified as the key active components of FZYAF, and TP53 was predicted as a core target. In vitro, UA and AHI inhibited PCa cell proliferation and migration and induced ferroptosis, with their combination showing enhanced efficacy compared to either agent alone. Mechanistically, UA and AHI were bound to and upregulated the TP53 protein. In vivo, FZYAF inhibited tumor growth and induced ferroptosis in PCa mice, which was associated with alterations in lipid metabolism-related pathways, as revealed. UA and AHI, key components of FZYAF, inhibit PCa progression by binding to and upregulating the TP53 protein to induce ferroptosis. This study elucidates the role of FZYAF in developing anti-PCa drugs. Supplementary Information: The online version contains supplementary material available at https://doi.org/10.1186/s12575-026-00357-x.
SN - 1480-9222
ER -