ArticleJournal of translational medicine2023
Cirsiliol induces autophagy and mitochondrial apoptosis through the AKT/FOXO1 axis and influences methotrexate resistance in osteosarcoma.
Article in Journal of translational medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 20 citations in OpenAlex.
- Engineered flavonoid disrupts mitochondrial AIF/CHCHD4 complex for targeted cancer therapy.Acta pharmaceutica Sinica. B · 2026Article
- Natural products mediate ferroptosis and immune microenvironment-linked sensitization in osteosarcoma: from chemotherapy resistance to combined therapeutic transformation.Molecular diversity · 2026Review
- Metabotyping ofPlants (Basel, Switzerland) · 2026Article
- Natural products reshape osteosarcoma cell fate: promoting cell death.Frontiers in pharmacology · 2026Review
- Cirsiliol alleviates diabetic cardiomyopathy by inhibiting oxidative stress and improving energy metabolism through the PPAR-α/AMPK pathway.Scientific reports · 2025Article
- PEA15 promotes osteosarcoma progression and cisplatin resistance by modulating autophagy through the FABP3-TNF signaling axis.iScience · 2025Article
- Unveiling the Chemical Profile of Teucrium chamaedrys subsp. gracile (Batt.) Rech.F. dried Aerial Parts From Algeria.Chemistry & biodiversity · 2025Article
- Cirsiliol alleviates experimental inflammatory bowel disease via restoration of intestinal barrier integrity and inhibition of NF-κB and MAPK pathways.Scientific reports · 2025Article
- Cirsiliol suppresses the proliferation of human oral cancer cells by targeting topoisomerase I.3 Biotech · 2025Article
- Sodium aescinate promotes apoptosis of pancreatic stellate cells and alleviates pancreatic fibrosis by inhibiting the PI3K/Akt/FOXO1 signaling pathways.Frontiers in pharmacology · 2025Article
- Cetrorelix promotes cell apoptosis via the PI3K-AKT-FOXO1 pathway in epithelial ovarian cancer.Frontiers in oncology · 2025Article
- Cirsiliol suppresses malignant progression of hepatocellular carcinoma via regulation of glutamine metabolism.American journal of translational research · 2025Article
- Muscle-specific lack of Gfpt1 triggers ER stress to alleviate misfolded protein accumulation.Disease models & mechanisms · 2024Article
- Trends and future directions of autophagy in osteosarcoma: A bibliometric analysis.Open medicine (Warsaw, Poland) · 2024Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundOsteosarcoma (OS) is the most common primary malignant bone tumor in children and adolescents, with poor outcomes for patients with metastatic disease or chemotherapy resistance. Cirsiliol is a recently found flavonoid with anti-tumor effects in various tumors. However, the effects of cirsiliol in the regulation of aggressive behaviors of OS remain unknown.
methodsThe effect of cirsiliol on the proliferation of OS cells was detected using a cell counting kit-8 (CCK-8) assay and 5-ethynyl-2'-deoxyuridine (EdU) staining, while cell apoptosis was detected using flow cytometry. Immunofluorescence was applied to visualize the expression level of the mitochondria, lysosomes and microtubule-associated protein light chain 3 (LC3). A computational molecular docking technique was used to predict the interaction between cirsiliol and the AKT protein. The impact of cirsiliol on resistance was investigated by comparing it between a methotrexate (MTX)-sensitive OS cell line, U2OS, and a MTX-resistant OS cell line, U2OS/MTX. Finally, in situ xenogeneic tumor models were used to validate the anti-tumor effect of cirsiliol in OS.
resultsCirsiliol inhibited cell proliferation and induced apoptosis in both U2OS and U2OS/MTX300 OS cells. In addition, treatment with cirsiliol resulted in G2 phase arrest in U2OS/MTX300 and U2OS cells. Cell fluorescence probe staining results showed impaired mitochondria and increased autophagy in OS cells after treatment with cirsiliol. Mechanistically, it was found that cirsiliol targeted AKT by reducing the phosphorylation of AKT, which further activated the transcriptional activity of forkhead Box O transcription factor 1 (FOXO1), ultimately affecting the function of OS cells. Moreover, in situ tumorigenesis experiments showed that cirsiliol inhibited the tumorigenesis and progression of OS in vivo.
conclusionsCirsiliol inhibits OS cell growth and induces cell apoptosis by reducing AKT phosphorylation and further promotes FOXO1 expression. These phenomena indicate that cirsiliol is a promising treatment option for OS.
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