Caspase-dependent apoptotic effect of shikonin in FaDu human head and neck squamous cell carcinomas
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Shikonin is being studied for its potential therapeutic effects on diseases owing to its biological and pharmacological activities, such as antioxidant, anti-inflammatory, antibacterial, antiviral, antiangiogenic, and wound-healing activities. However, its effectiveness in treating oral cancer is still uncertain. This study investigated the effect of shikonin on apoptosis in FaDu human pharyngeal carcinoma cells by employing 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide (MTT) assays and Western blot analyses. The MTT assay revealed that shikonin promoted apoptosis in FaDu cells in a dose-dependent manner. Shikonin-induced apoptosis in FaDu cells was mediated by Fas expression and activation of caspase-8, caspase-3, and PARP. Western blot analysis showed a downregulation of Bcl-xl and Bcl-2, as well as an upregulation of Bax and Bad in FaDu cells treated with shikonin acid. These findings indicate that shikonin inhibits the proliferation of FaDu human pharyngeal carcinoma cells and induces apoptosis through both the cell death receptor-mediated extrinsic and mitochondrial-mediated intrinsic pathways.
Abstract
Shikonin is being studied for its potential therapeutic effects on diseases owing to its biological and pharmacological activities, such as antioxidant, anti-inflammatory, antibacterial, antiviral, antiangiogenic, and wound-healing activities. However, its effectiveness in treating oral cancer is still uncertain. This study investigated the effect of shikonin on apoptosis in FaDu human pharyngeal carcinoma cells by employing 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide (MTT) assays and Western blot analyses. The MTT assay revealed that shikonin promoted apoptosis in FaDu cells in a dose-dependent manner. Shikonin-induced apoptosis in FaDu cells was mediated by Fas expression and activation of caspase-8, caspase-3, and PARP. Western blot analysis showed a downregulation of Bcl-xl and Bcl-2, as well as an upregulation of Bax and Bad in FaDu cells treated with shikonin acid. These findings indicate that shikonin inhibits the proliferation of FaDu human pharyngeal carcinoma cells and induces apoptosis through both the cell death receptor-mediated extrinsic and mitochondrial-mediated intrinsic pathways.