PDF(Pubmed)
Abstract：
A balance on nutrient supply and redox homeostasis is required for cell survival, and increased antioxidant capacity of cancer cells may lead to chemotherapy failure.
To investigate the mechanism of anti-proliferation of cardamonin by inducing oxidative stress in ovarian cancer cells.
After 24 h of drug treatment, CCK8 kit and wound healing test were used to detect cell viability and migration ability, respectively, and the ROS levels were detected by flow cytometry. The differential protein expression after cardamonin administration was analyzed by proteomics, and the protein level was detected by Western blotting.
Cardamonin inhibited the cell growth, which was related to ROS accumulation. Proteomic analysis suggested that MAPK pathway might be involved in cardamonin-induced oxidative stress. Western blotting showed that cardamonin decreased Raptor expression and the activity of mTORC1 and ERK1/2. Same results were observed in Raptor KO cells. Notably, in Raptor KO cells, the effect of cardamonin was weakened.
Raptor mediated the function of cardamonin on cellular redox homeostasis and cell proliferation through mTORC1 and ERK1/2 pathways.
To investigate the mechanism of anti-proliferation of cardamonin by inducing oxidative stress in ovarian cancer cells.
After 24 h of drug treatment, CCK8 kit and wound healing test were used to detect cell viability and migration ability, respectively, and the ROS levels were detected by flow cytometry. The differential protein expression after cardamonin administration was analyzed by proteomics, and the protein level was detected by Western blotting.
Cardamonin inhibited the cell growth, which was related to ROS accumulation. Proteomic analysis suggested that MAPK pathway might be involved in cardamonin-induced oxidative stress. Western blotting showed that cardamonin decreased Raptor expression and the activity of mTORC1 and ERK1/2. Same results were observed in Raptor KO cells. Notably, in Raptor KO cells, the effect of cardamonin was weakened.
Raptor mediated the function of cardamonin on cellular redox homeostasis and cell proliferation through mTORC1 and ERK1/2 pathways.
摘要：
■细胞存活需要营养供应和氧化还原稳态的平衡，癌细胞抗氧化能力的增加可能导致化疗失败。
■目的探讨豆蔻素诱导卵巢癌细胞氧化应激抑制增殖的机制。
■药物治疗24小时后，CCK8试剂盒和伤口愈合试验检测细胞活力和迁移能力,分别,流式细胞仪检测ROS水平。通过蛋白质组学分析豆蔻素给药后的差异蛋白表达，蛋白质水平通过蛋白质印迹法检测。
■Cardamonin抑制细胞生长，这与ROS积累有关。蛋白质组学分析表明MAPK通路可能参与了豆蔻素诱导的氧化应激。Westernblotting结果显示，豆蔻素降低了Raptor的表达以及mTORC1和ERK1/2的活性。在RaptorKO细胞中观察到相同的结果。值得注意的是,在RaptorKO细胞中，豆蔻素的作用减弱。
■Raptor通过mTORC1和ERK1/2途径介导了豆蔻素对细胞氧化还原稳态和细胞增殖的功能。
■目的探讨豆蔻素诱导卵巢癌细胞氧化应激抑制增殖的机制。
■药物治疗24小时后，CCK8试剂盒和伤口愈合试验检测细胞活力和迁移能力,分别,流式细胞仪检测ROS水平。通过蛋白质组学分析豆蔻素给药后的差异蛋白表达，蛋白质水平通过蛋白质印迹法检测。
■Cardamonin抑制细胞生长，这与ROS积累有关。蛋白质组学分析表明MAPK通路可能参与了豆蔻素诱导的氧化应激。Westernblotting结果显示，豆蔻素降低了Raptor的表达以及mTORC1和ERK1/2的活性。在RaptorKO细胞中观察到相同的结果。值得注意的是,在RaptorKO细胞中，豆蔻素的作用减弱。
■Raptor通过mTORC1和ERK1/2途径介导了豆蔻素对细胞氧化还原稳态和细胞增殖的功能。
