ArticleCancer cell international2025
Comprehensive network pharmacology and experimental study to investigate the effect and mechanism of solasonine on breast carcinoma treatment.
Article in Cancer cell international, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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Who cites it
3 citing papers in PubMed.
- Solasonine suppresses non-small cell lung cancer progression by inhibiting the STAT3/PD-L1 axis.Scientific reports · 2026Article
- Targeting SRC to mediate solasonine's anti-cancer activity in hepatocellular carcinoma and its potential for multi-cancer therapy.Frontiers in oncology · 2026Article
- Click synthesis of some novel benzo[RSC medicinal chemistry · 2025Article
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundFerroptosis is a therapeutic strategy for breast carcinoma (BC). Solasonine (SS) was linked to ferroptosis as a tumor suppressor. However, whether SS could treat BC by activating ferroptosis and its underlying mechanisms has not been reported.
methodsWe obtained the intersection of genes targeting SS and BC disease through network pharmacology. Bioinformatics analysis revealed that the intersection genes were primarily enriched in the extracellular signal-regulated kinase 2/mitogen-activated protein kinase (ERK2/MAPK) signaling pathway. The interaction modes of SS with ERK2 and epidermal growth factor receptor (EGFR) were simulated by molecular docking. We further detected the expressions of ERK2 and p-ERK2 in BC patients and the correlation between ERK2/p-ERK2 and ferroptosis. The effects and mechanism of SS on ferroptosis in BC were validated by mutation plasmids construction, immunohistology, wound healing, transwell assay, and western blotting using in vitro and in vivo models.
resultsERK2 and p-ERK2 were up-regulated in BC patients, and the ERK2/p-ERK2 ratio was negatively correlated with ferroptosis. Molecular docking indicated that SS could bind to ERK2 and EGFR to inhibit the activity of the ERK2/MAPK pathway. In vitro and in vivo experiments confirmed that SS induced ferroptosis by inhibiting the ERK2/MAPK pathway, inhibiting proliferation, migration, and invasion of BC cells.
conclusionSS could inactivate the ERK2/MAPK pathway, thereby inducing ferroptosis and further inhibiting BC cell proliferation, migration, and invasion. This study clarified the potential mechanism of SS in BC and provided a theoretical basis for its clinical application.
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