ArticleAnti-cancer drugs2016
Tectorigenin inhibits osteosarcoma cell migration through downregulation of matrix metalloproteinases in vitro.
Article in Anti-cancer drugs, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 28 citations in OpenAlex.
- Traditional Uses, Phytochemistry, Pharmacology, and Toxicology ofPlants (Basel, Switzerland) · 2025Review
- Neuroprotective Effects of Tectoridin in HNeurochemical research · 2025Article
- Article
- Tectorigenin Inhibits Glycolysis-induced Cell Growth and Proliferation by Modulating LncRNA CCAT2/miR-145 Pathway in Colorectal Cancer.Current cancer drug targets · 2024Article
- Tectorigenin: A Review of Its Sources, Pharmacology, Toxicity, and Pharmacokinetics.Molecules (Basel, Switzerland) · 2023Review
- Cytotoxic Compounds fromMolecules (Basel, Switzerland) · 2023Article
- Cyclic Stretch-Induced Mechanical Stress Applied at 1 Hz Frequency Can Alter the Metastatic Potential Properties of SAOS-2 Osteosarcoma Cells.International journal of molecular sciences · 2023Article
- Antitumor effects and mechanisms of pyropheophorbide‑α methyl ester‑mediated photodynamic therapy on the human osteosarcoma cell line MG‑63.International journal of molecular medicine · 2020Article
- Glycogen synthase kinase 3β as a potential therapeutic target in synovial sarcoma and fibrosarcoma.Cancer science · 2020Article
- Anti-Endometriotic Effects of Pueraria Flower Extract in Human Endometriotic Cells and Mice.Nutrients · 2017Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tectorigenin (Tec) is an effective component of the traditional Chinese medicine Belamcanda chinensis, which has been reported to exert beneficial effects in various types of cancer. However, the activity and mechanism of Tec in osteosarcoma (OS) have not been investigated to date. The aim of the present study was to examine the inhibitory effect of Tec on OS and its underlying mechanism of action. OS cells (Saos2 and U2OS) were treated with various concentrations of Tec for 24, 48, and 72 h. Cell proliferation was evaluated using an CCK-8 assay. Cell migration and invasion ability were measured using the Transwell assay. The expressions of MMP1, MMP2, MMP9, and cleaved caspase3 were measured using real-time PCR and/or western blot analysis. We found that Tec inhibited the proliferation of OS cells (Saos2 and U2OS) in a dose-dependent and time-dependent manner. In addition, Tec significantly inhibited migration and invasion in OS cells (P<0.05). Tec upregulated the expression of cleaved caspase3, while downregulating the expression of MMP1, MMP2, and MMP9. Taken together, the present study provided fundamental evidence for the application of Tec in chemotherapy against OS.
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