Eupatilin reduces cell viability by 50 μM in YD-10B cells, indicating potent anti-invasive and apoptotic activity against oral squamous cell carcinoma.
Oral squamous cell carcinoma (OSCC) is an aggressive malignancy characterized by high invasiveness and poor prognosis. This study investigated the anticancer mechanisms of eupatilin, a pharmacologically active flavonoid derived from Artemisia species, in human OSCC YD-10B cells. Eupatilin significantly reduced cell viability in a dose-dependent manner, with an IC50 of approximately 50 μM. Flow cytometric analysis revealed G0/G1 phase arrest accompanied by downregulation of Cyclin D1 and CDK2, and upregulation of p21. Annexin V/Propidium Iodide staining and Western blotting confirmed apoptosis induction through activation of Bax, cleaved caspase-3/9, and poly ADP-ribose polymerase (PARP) cleavage, alongside suppression of Bcl-2. Furthermore, eupatilin markedly decreased both the mRNA expression and enzymatic activities of matrix metalloproteinases (MMP)-2 and MMP-9, indicating its potential to inhibit cancer cell invasion. Collectively, these findings demonstrate that eupatilin exerts potent antiproliferative and anti-invasive effects on OSCC cells via cell-cycle modulation and mitochondrial-mediated apoptosis. This study provides the first evidence of eupatilin’s therapeutic potential against OSCC, suggesting its promise as a natural compound for the development of safer and more effective treatments for oral cancer.
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Suk‐Yul Jung (2025) studied this question.
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