ArticleInternational journal of immunopathology and pharmacology
Curcumin suppresses metastasis, invasion, and proliferation in osteosarcoma cells by regulating the EGFR/Src signaling axis.
Article in International journal of immunopathology and pharmacology. 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.
- A 'three-axis synergy' immunotherapeutic strategy for malignant bone tumors based on natural bioactives and bioactive materials.Bioactive materials · 2026Review
- Repurposing trifluoperazine as a potential therapeutic agent for ovarian cancer: mechanistic insight via SRC/PI3K/AKT signaling pathway inhibition.Journal of ovarian research · 2026Article
- Mycl, activated by Sgk1-phosphorylated Stat3, mediates osteoclastogenesis via Ctsk transcriptional regulation.Scientific reports · 2025Article
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6 authors.
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Abstract
We explored the biological mechanisms by which curcumin (Cur) confronts osteosarcoma (OS) tumorigenesis and potential drug gene targets based on network pharmacology and in vitro cell experiments. Cur has been recognized for its significant role in combating various types of tumors. However, the intrinsic molecular mechanisms through which it affects OS remain uncharted. In this study, we performed network pharmacology methods including protein-protein interaction (PPI) and core target screening, Functional Enrichment Analysis and Network Construction, Molecular Docking, which obtained the potential target of Cur. Meanwhile, cell experiments (wound healing assay, Transwell assay, Western blots, immunofluorescence, et al.) in vitro were performed to verify the targets, and reveal the biological mechanisms. A total of 18 hub genes were identified through our network pharmacological analysis. In vitro studies show that Cur inhibits the proliferation, migration, invasion capabilities of MG63 and U2OS cells. Western blot reveals a down-regulation of p-PI3K, PI3K, p-Akt, Akt, EGFR, Src, p-Src (Tyr416) and STAT3 expression when treated with Cur. Additionally, Cur upregulated epithelial proteins (E-cadherin and Occludin) while decreasing the expression of the mesenchymal protein (N-cadherin). In addition, Cur treatment decreases the EGFR/Src signaling pathway in the presence of active Src overexpression. Cur inhibits the proliferation, migration, invasion, epithelial-mesenchymal transition (EMT) by down-regulating EGFR/Src signaling axis, also resulting in coordinated weakening of its downstream regulatory genes, including Akt, STAT3, Bcl2, ERK1/2, among others signal axis (PI3K/Akt signaling pathway).
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