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<p>Oral cancer poses a significant global health challenge, with increasing incidence rates and substantial morbidity and mortality. This study aimed to investigate the antiproliferative effects of cirsiliol in human oral cancer cells. Results from the MTT cell viability assay showed that cirsiliol significantly (<i>p</i> &lt; 0.05) inhibited the growth of all oral cancer cell lines tested, with the IC<sub>50</sub> values ranging from 12 to 25&#xa0;μM. The lowest IC<sub>50</sub> of 12&#xa0;μM was observed against SCC-1 and SCC-25 cell lines, while the IC<sub>50</sub> for normal hTRET-OME cells was 75&#xa0;μM, approximately 6 times higher than against the oral cancer cells. Further molecular analysis revealed that cirsiliol disrupted cellular morphology in SCC-1 and SCC-25 cells with minor effects on the normal hTRET-OME cells. Annexin V/PI staining indicated that the percentage of SCC-1 and SCC-25 apoptotic cells increased significantly from 4.70 and 5.27% in controls to 31.4 and 35.28% at 24&#xa0;μM cirsiliol, respectively. This effect correlated with an upregulation of Bax, downregulation of Bcl-2, and increased p53 expression. Nonetheless, the apoptotic effects of cirsiliol were considerably lower in normal hTRET-OME cells. Western blotting together with molecular docking analysis suggested that cirsiliol may inhibit the expression of topoisomerase I. Additionally, wound healing and transwell assays demonstrated that cirsiliol significantly (<i>p</i> &lt; 0.05) suppressed the migration and invasion of SCC-1 and SCC-25 cells. In conclusion, these findings indicate that cirsiliol induces apoptosis in oral cancer cells through the inhibition of topoisomerase I.</p>

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Cirsiliol suppresses the proliferation of human oral cancer cells by targeting topoisomerase I

  • 期刊论文

  • 发表日期：

    2025年2月21日

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  • Ping Xu,
  • Jun Chen,
  • Dongwen Li,
  • Lu Shen,
  • Yangyi Zhang,
  • Ruiting Peng,
  • Yong He

摘要

Oral cancer poses a significant global health challenge, with increasing incidence rates and substantial morbidity and mortality. This study aimed to investigate the antiproliferative effects of cirsiliol in human oral cancer cells. Results from the MTT cell viability assay showed that cirsiliol significantly (p < 0.05) inhibited the growth of all oral cancer cell lines tested, with the IC50 values ranging from 12 to 25 μM. The lowest IC50 of 12 μM was observed against SCC-1 and SCC-25 cell lines, while the IC50 for normal hTRET-OME cells was 75 μM, approximately 6 times higher than against the oral cancer cells. Further molecular analysis revealed that cirsiliol disrupted cellular morphology in SCC-1 and SCC-25 cells with minor effects on the normal hTRET-OME cells. Annexin V/PI staining indicated that the percentage of SCC-1 and SCC-25 apoptotic cells increased significantly from 4.70 and 5.27% in controls to 31.4 and 35.28% at 24 μM cirsiliol, respectively. This effect correlated with an upregulation of Bax, downregulation of Bcl-2, and increased p53 expression. Nonetheless, the apoptotic effects of cirsiliol were considerably lower in normal hTRET-OME cells. Western blotting together with molecular docking analysis suggested that cirsiliol may inhibit the expression of topoisomerase I. Additionally, wound healing and transwell assays demonstrated that cirsiliol significantly (p < 0.05) suppressed the migration and invasion of SCC-1 and SCC-25 cells. In conclusion, these findings indicate that cirsiliol induces apoptosis in oral cancer cells through the inhibition of topoisomerase I.