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Published on: October 10, 2025
Targeting FOXM1/PSAT1 axis by Brusatol inhibits lung cancer malignant progression
Siyi Ou1, Xiaobo Wang2, Yulan Sun2
1Department of Respiratory and Critical Care Medicine, The First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi 530021, China; Department of Respiratory and Critical Care Medicine, the First People's Hospital of Qinzhou, Qinzhou, Guangxi 535000, China.
Abstract:
Brusatol (BRU), an extract from Brucea javanica, has been found to inhibit cancer progression. However, the downstream targets of Brusatol and its underlying mechanisms in lung cancer still not fully elucidate and warrant further investigation. Here, we identified that Brusatol significantly downregulated the mRNA and protein levels of phosphoserine aminotransferase 1 (PSAT1). Notably, overexpression of PAST1 could impair the antitumour effects of Brusatol on lung cancer cells in vitro and in vivo. Further mechanism studies revealed that FOXM1, an important transcription factor, was directly bound to the promoter of PSAT1, facilitating its transcription. Besides, FOXM1 upregulation antagonizes Brusatol's suppression of PSAT1 and sustains tumor cell viability. Collectively, our data suggested that the FOXM1/PSAT1 axis might play an important role in the antitumour effects of Brusatol and that Brusatol may hold promise as a novel therapeutic strategy for lung cancer.
Insights
Brusatol, a compound from Brucea javanica, inhibits lung cancer by downregulating phosphoserine aminotransferase 1 (PSAT1). The FOXM1/PSAT1 pathway is key to Brusatol
Area of Science:
- Oncology
- Molecular Biology
- Pharmacology
Background:
- Brusatol (BRU), derived from Brucea javanica, exhibits anti-cancer properties.
- The precise mechanisms of Brusatol's action in lung cancer remain incompletely understood.
- Identifying downstream targets is crucial for understanding Brusatol's therapeutic potential.
Purpose of the Study:
- To elucidate the downstream targets and mechanisms of Brusatol in lung cancer.
- To investigate the role of phosphoserine aminotransferase 1 (PSAT1) in Brusatol's anti-cancer effects.
- To explore the involvement of the transcription factor FOXM1 in regulating PSAT1.
Main Methods:
- Quantitative real-time PCR and Western blotting to assess mRNA and protein levels.
- In vitro and in vivo experiments to evaluate the impact of PSAT1 overexpression on Brusatol's efficacy.
- Chromatin immunoprecipitation assays to determine FOXM1 binding to the PSAT1 promoter.
Main Results:
- Brusatol significantly reduced both mRNA and protein expression of PSAT1.
- Overexpression of PSAT1 counteracted the anti-tumor effects of Brusatol in lung cancer cells.
- FOXM1 directly binds to the PSAT1 promoter, enhancing its transcription.
- FOXM1 upregulation abrogated Brusatol's inhibitory effects on PSAT1 and promoted tumor cell survival.
Conclusions:
- The FOXM1/PSAT1 axis is identified as a critical mediator of Brusatol's anti-cancer activity in lung cancer.
- Brusatol demonstrates potential as a novel therapeutic strategy for lung cancer by targeting the FOXM1/PSAT1 pathway.
- Further research into this pathway could lead to improved lung cancer treatments.
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