ArticleFrontiers in pharmacology2025
Dual-edged mechanisms of α-tomatine in hepatocellular carcinoma by suppression of Wnt/β-catenin signaling versus RelB-Driven resistance in tumor therapy.
Article in Frontiers in pharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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Who cites it
1 citing paper in PubMed.
- Anti-inflammatory activity of α-tomatineInternational journal of medical sciences · 2026Article
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4 authors.
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Abstract
Background: The plant-derived steroidal alkaloid α-tomatine has emerged as a promising pan-cancer therapeutic agent, its multifaceted biological effects in HCC remain unexplored. This study aims to decipher α-tomatine's molecular duality in HCC, resolving its paradoxical capacity to simultaneously activate tumor-suppressive signaling and provoke chemoresistance networks, ultimately establishing synergistic phytotherapy strategies. Methods: HepG2 and SMMC-7721 hepatocellular carcinoma cells were exposed to α-tomatine to evaluate dose-dependent effects on proliferation, migration/invasion, and cell cycle distribution. Transcriptomic profiling via RNA sequencing identified dysregulated pathways. Pharmacological interventions using Wnt3a (activation) and XAV939 (inhibition) modulated Wnt/β-catenin signaling, while CRISPR/Cas9-mediated Results: α-Tomatine demonstrated dose-dependent suppression of hepatocellular carcinoma cell proliferation, migration, and invasion, concomitant with G2/M phase arrest. Mechanistically, it exerted Wnt/β-catenin inhibition via β-catenin phosphorylation/degradation while paradoxically inducing RelB-mediated reduction of anti-tumor activity. Wnt activation attenuated therapeutic effects, whereas Wnt inhibitors enhanced efficacy. Genetic RelB ablation potentiated α-tomatine's anti-tumor activity, contrasting with resistance in RelB-overexpressing models. Xenografts confirmed enhanced suppression in RelB-deficient tumors. Conclusion: This plant-derived alkaloid exerts anti-HCC effects through Wnt pathway modulation, while compensatory RelB activation constrains therapeutic outcomes. Strategic RelB co-targeting establishes a dual pathway phytotherapy paradigm, synergistically merging botanical pharmacodynamics with precision oncology.
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