ArticleDiscover oncology2025
Isorhamnetin inhibits cholangiocarcinoma proliferation and metastasis via PI3K/AKT signaling pathway.
Article in Discover oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Exploring the immunomodulatory mechanisms of Astragalus membranaceus in esophageal cancer treatment through network pharmacology, molecular docking, and molecular dynamics simulation.Discover oncology · 2026Article
- Isorhamnetin from Astragalus membranaceus exerts anti-glioma effects via PI3K/Akt signaling pathway.American journal of cancer research · 2026Article
- Isorhamnetin: Reviewing Recent Developments in Anticancer Mechanisms and Nanoformulation-Driven Delivery.International journal of molecular sciences · 2025Review
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Authors and funding
7 authors.
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Abstract
backgroundCholangiocarcinoma (CCA), which is a malignant tumor originating from the epithelial cells of the bile ducts, has witnessed an increasing incidence year by year. Owing to the dearth of effective treatments, the prognosis for CCA is rather poor. Isorhamnetin is known to possess anti-tumor, anti-inflammatory and oxidative stress modulating effects; however, its role in CCA remains unclear.
methodsFirstly, we screened the core targets and pathways of isorhamnetin for the treatment of CCA through a network pharmacology approach. Subsequently, we verified via molecular docking that the core targets could dock stably with isorhamnetin. Finally, we verified the inhibitory effect of isorhamnetin on the malignant biological behavior of CCA in vitro and in vivo experiments.
resultsBased on the network pharmacology analysis, we came to the conclusion that AKT1 might be a core target of isorhamnetin in the treatment of CCA. Molecular docking indicated that AKT1 was capable of binding stably to isorhamnetin. Subsequently, In vitro experiments demonstrated that isorhamnetin was able to suppress the proliferation and metastasis of CCA cells, and AKT1 played a pivotal role in this process. Mechanistically speaking, isorhamnetin exerts its inhibitory effect on tumor growth via the PI3K/AKT signaling pathway.
conclusionsOur study demonstrated for the first time that isorhamnetin can inhibit the progression of CCA through PI3K/AKT, and that AKT1 may be a target of isorhamnetin for the treatment of CCA.
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