Abstract: SA-PO1262
Magnolin Inhibits Renal Carcinoma Cell Metastasis by Targeting TGF-β1/SMAD/AP1-Mediated MMP-9 Expression
Session Information
- Onconephrology: Epidemiological Trends, Risk Stratification, and Clinical Outcomes
October 24, 2026 | Location: Exhibit Hall A, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Onconephrology
- 1600 Onconephrology
Authors
- Tsai, Jen Pi, Dalin Tzu Chi Hospital, Dalin, Taiwan Province, Taiwan
- Hsieh, Yi-Hsien, Chung Shan Medical University, Taichung, Taichung City, Taiwan
Background
Over the past decade, renal carcinoma cell (RCC) incidence has increased markedly. Targeted and immune therapies for advanced disease often cause nephrotoxicity. Thus, developing effective therapies with minimal renal toxicity is a priority. Magnolin, from Magnolia officinalis, shows anti-inflammatory and anti-cancer effects. However, its antitumor effects on RCC cells and underlying mechanisms remain unclear.
Methods
Cell viability, migration, and invasion were evaluated by MTT, flow cytometry, colony formation, and Transwell assays. Gene and protein expression were analyzed by qRT-PCR and western blotting. TCGA identified MMP9/TGF-β1 as targets. Immunofluorescence and ChIP confirmed pathway regulation. In vivo assays validated anti-metastatic efficacy and safety.
Results
Magnolin suppresses RCC cell proliferation, migration, and invasion, likely via downregulation of MMP-9. Magnolin inhibits TGF-β1 transcription and translation, blocks SMAD2/3 phosphorylation and nuclear translocation, and reduces AP-1 (c-Jun/c-Fos) expression, thereby decreasing MMP-9 transcriptional activity. Consequently, Magnolin inhibits RCC cell migartion and invasion. In vivo, it significantly reduces lung metastasis without evident systemic toxicity.
Conclusion
This study provides the first key evidence that Magnolin suppresses renal cell carcinoma metastasis by targeting the TGF-β1/SMAD/AP1-mediated MMP-9 pathway, supporting its potential as a natural therapeutic agent against RCC.
Funding
- Other NIH Support