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ARTICLE

Ugonin J Inhibits EMT and Migration in Prostate Cancer by Suppressing ADAM9 Expression

Jo-Yu Lin1,#, Tien-Huang Lin2,3,#, Ya-Jing Jiang4, Liang-Wei Lin4, Kuan-Ying Lai5, Yi-Chin Fong6,7,8, Chih-Chuang Liaw5,9,*, Chih-Hsin Tang1,4,10,11,*
1 Graduate Institute of Biomedical Sciences, China Medical University, Taichung, 404333, Taiwan
2 School of Post-Baccalaureate Chinese Medicine, Tzu Chi University, Hualien, 970374, Taiwan
3 Department of Urology, Buddhist Tzu Chi General Hospital Taichung Branch, Taichung, 427213, Taiwan
4 Department of Pharmacology, School of Medicine, China Medical University, Taichung, 404333, Taiwan
5 Department of Marine Biotechnology and Resources, National Sun Yat-Sen University, Kaohsiung, 804201, Taiwan
6 Department of Sports Medicine, College of Health Care, China Medical University, Taichung, 404333, Taiwan
7 Department of Orthopedic Surgery, China Medical University Hospital, Taichung, 404333, Taiwan
8 Department of Orthopedic Surgery, China Medical University Beigang Hospital, Yunlin, 651012, Taiwan
9 Graduate Institute of Natural Products, Kaohsiung Medical University, Kaohsiung, 807378, Taiwan
10 Department of Medical Laboratory Science and Biotechnology, Asia University, Taichung, 413305, Taiwan
11 Chinese Medicine Research Center, China Medical University, Taichung, 404333, Taiwan
* Corresponding Author: Chih-Chuang Liaw. Email: email; Chih-Hsin Tang. Email: email
# These authors contributed equally to this work
(This article belongs to the Special Issue: Advancements in Molecular Therapeutics for Prostate Cancer)

Oncology Research https://doi.org/10.32604/or.2025.074202

Received 05 October 2025; Accepted 12 November 2025; Published online 29 December 2025

Abstract

Background: Prostate cancer (PCa) is the most prevalent malignancy in men and often correlates with distant metastasis in its advanced stages. The study aimed to investigate the effects of Ugonin J, a natural compound isolated from Helminthostachys zeylanica, on PCa metastasis. Methods: The effects of Ugonin J on cell motility were assessed using migration and invasion assays. Reverse Transcription Quantitative PCR (RT-qPCR) and Western blotting were used to evaluate the impact of Ugonin J on mRNA and protein expression. RNA sequencing (RNA-seq) analysis was performed to investigate candidate mechanisms. Differential gene expression analysis in PCa patients was conducted using multiple databases. Results: Here, we reveal that Ugonin J blocks migration and invasion in PCa cells without affecting cell viability. RNA-seq analysis suggests that epithelial–mesenchymal transition (EMT) is potentially involved in Ugonin J’s anti-motility effects. Ugonin J also suppresses the expression of mesenchymal markers N-cadherin, β-catenin, Snail, and Slug while upregulating the expression of the epithelial marker E-cadherin. Furthermore, among 13 A disintegrin and metalloproteinase (ADAM) proteins, A disintegrin and metalloproteinase domain-containing protein 9 (ADAM9) is the most downregulated following Ugonin J treatment, according to our RNA-seq data. Importantly, clinical data revealed that ADAM9 expression are higher in PCa patients than in healthy controls and are associated with distant metastasis. Transfection with ADAM9 cDNA reverses Ugonin J-regulated downregulation of EMT, migration, and invasion in PCa cells. Ugonin J inhibits ADAM9-dependent motility by downregulating the phosphoinositide 3-kinase (PI3K), protein kinase B (Akt) and nuclear factor-κB (NF-κB) pathways. Conclusions: Our evidence suggests that Ugonin J is a novel therapeutic candidate for further development as a treatment for metastatic PCa.

Keywords

Prostate cancer; Ugonin J; epithelial–mesenchymal transition (EMT); a disintegrin and metalloproteinase domain-containing protein 9 (ADAM9)

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