Archives of oral biology · 2020
Cordycepin induces apoptosis in human tongue cancer cells in vitro and has antitumor effects in vivo.
СтатьяНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Zheng Qingwei, Sun Jing, Li Wenli, Li Shuangnan, Zhang Kai
Аннотация
OBJECTIVE: This study was designed to explore the ability of cordycepin to disrupt human tongue cancer cell growth, and to assess the mechanistic basis for such anti-cancer activity.
METHODS: CAL-27 human tongue cancer cells were treated with cordycepin prior to analysis via CCK-8 assay in order to assess their proliferation. In addition, cell cycle progression and apoptotic death in these cells were measured via flow cytometry, while the expression of apoptosis-associated genes and proteins (caspase-3, caspase-9, caspase-12, Bcl-2, and Bax) were measured via real-time PCR and western blotting. We further measured the intracellular production of reactive oxygen species (ROS) and used a murine xenograft model system to explore the in vivo anti-tumor activity of cordycepin.
RESULTS: Cordycepin was able to significantly suppress the proliferation of CAL-27 cells in a dose-dependent fashion (IC50 = 40 μg/mL at 24 h). Cordycepin further induced Bax, caspase-3, caspase-9, and caspase-12 upregulation at the mRNA and protein levels while simultaneously downregulating anti-apoptotic Bcl-2 expression. CAL-27 cells treated using cordycepin also exhibited elevated levels of intracellular ROS. Importantly, cordycepin was able to effectively suppress tongue cancer tumor growth in a murine xenograft model system and similar mRNA and protein levels were observed in vivo.
CONCLUSIONS: Cordycepin can inhibit human tongue cancer cell growth and can drive their apoptotic death via the mitochondrial pathway. In addition, cordycepin can suppress tongue cancer growth in vivo in treated mice.
METHODS: CAL-27 human tongue cancer cells were treated with cordycepin prior to analysis via CCK-8 assay in order to assess their proliferation. In addition, cell cycle progression and apoptotic death in these cells were measured via flow cytometry, while the expression of apoptosis-associated genes and proteins (caspase-3, caspase-9, caspase-12, Bcl-2, and Bax) were measured via real-time PCR and western blotting. We further measured the intracellular production of reactive oxygen species (ROS) and used a murine xenograft model system to explore the in vivo anti-tumor activity of cordycepin.
RESULTS: Cordycepin was able to significantly suppress the proliferation of CAL-27 cells in a dose-dependent fashion (IC50 = 40 μg/mL at 24 h). Cordycepin further induced Bax, caspase-3, caspase-9, and caspase-12 upregulation at the mRNA and protein levels while simultaneously downregulating anti-apoptotic Bcl-2 expression. CAL-27 cells treated using cordycepin also exhibited elevated levels of intracellular ROS. Importantly, cordycepin was able to effectively suppress tongue cancer tumor growth in a murine xenograft model system and similar mRNA and protein levels were observed in vivo.
CONCLUSIONS: Cordycepin can inhibit human tongue cancer cell growth and can drive their apoptotic death via the mitochondrial pathway. In addition, cordycepin can suppress tongue cancer growth in vivo in treated mice.