ArticleFrontiers in pharmacology2025
Cardamonin induces apoptosis of colorectal cancer cells via targeted inhibition of the JAK/STAT3/epithelial-mesenchymal transition (EMT) signaling axis.
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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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- Ultrasound-Assisted Ternary Deep Eutectic Solvent Extraction of Total Flavonoids fromAntioxidants (Basel, Switzerland) · 2026Article
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6 authors.
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Abstract
Background: Colorectal cancer (CRC) remains a leading cause of cancer-related morbidity and mortality worldwide. Cardamonin (CDN), a bioactive flavonoid derived from the seeds of Methods: Network pharmacology and molecular docking were employed to identify signaling pathways and targets associated with the anti-CRC activity of CDN. Cell viability, proliferation, migration, and invasion were evaluated using CCK-8, EdU, wound healing, and Transwell assays, respectively. Apoptosis and cell cycle were analyzed by flow cytometry. Proteomic profiling was applied to explore the underlying mechanisms, and the findings were validated using Western blot and functional assays. The antitumor efficacy of CDN Results: JAK1, STAT3, AKT1, EGFR, IL1B, and ESR1 were identified as shared core targets. The JAK/STAT3 pathway and apoptosis were recognized as pivotal mechanisms mediating the anti-CRC effects of CDN. Conclusions: CDN inhibits CRC progression and induces apoptosis by targeting the JAK/STAT3/EMT signaling axis, suggesting that CDN is a promising therapeutic agent for CRC.
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