ArticleJournal of Cancer2022
Silibinin inhibits the migration, invasion and epithelial-mesenchymal transition of prostate cancer by activating the autophagic degradation of YAP.
Article in Journal of Cancer, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Nano-silymarin combined with methylene blue photodynamic therapy versus monotherapies of head and neck squamous cell carcinoma: in-vitro study.BMC cancer · 2026Article
- Programmed cell death mechanisms of traditional plant medicine in prostate cancer therapy.Frontiers in immunology · 2026Review
- Effect of HIF-1α and LDHA Blockade on Gene Expression of Tumor Immune Evasion in Myeloid Leukemia Cell Lines.Iranian biomedical journal · 2026Article
- Natural anti-cancer products: insights from herbal medicine.Chinese medicine · 2025Review
- Silybin-Functionalized PCL Electrospun Fibrous Membranes for Potential Pharmaceutical and Biomedical Applications.Polymers · 2024Article
- A review of the botany, phytochemistry, pharmacology, synthetic biology and comprehensive utilization ofFrontiers in pharmacology · 2024Review
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Authors and funding
9 authors.
Funding
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Abstract
Silibinin (SB), a flavonoid extracted from milk thistle seeds, has been found to exert antitumor effects in numerous tumor types. Our previous study reported that SB had anti-metastatic effects in prostate cancer (PCa). However, the exact underlying molecular mechanisms remain to be determined. The present study aimed to investigate the effects of SB on the migration, invasion and epithelial-mesenchymal transition (EMT) of castration-resistant PCa (CRPC) cells using wound healing, Transwell assays, and western blotting. The results revealed that SB treatment significantly inhibited the migration and invasion of CRPC cell lines. Moreover, SB was confirmed to activate autophagy, as determined using LC3 conversion, LC3 turnover and LC3 puncta assays. Further mechanistic studies indicated that the expression levels of Yes-associated protein (YAP) were downregulated in an autophagy-dependent manner after SB treatment. In addition, the SB-induced autophagic degradation of YAP was associated with the anti-metastatic effects of SB in CRPC. In conclusion, the findings of the present study suggested that SB might inhibit the migration, invasion and EMT of PCa cells by regulating the autophagic degradation of YAP, thus representing a potential novel treatment strategy for metastatic CRPC.
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