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Oxidative stress induced by carboplatin promotes apoptosis and inhibits migration of HN-3 cells

机译:卡铂诱导的氧化应激促进细胞凋亡并抑制HN-3细胞迁移

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摘要

Laryngeal squamous cell carcinoma (LSCC) is currently a serious public health problem in China; thus, it is urgent to identify effective treatment strategies for this disease. Previous studies demonstrated that reactive oxygen species (ROS) serve important roles in the apoptosis of LSCC cells. It has also been indicated that carboplatin (CBDCA), a second-generation platinum compound with broad antineoplastic properties, is able to induce oxidative stress to produce ROS, which in turn promotes apoptosis. Thus, the present study investigated if CBDCA is cytotoxic in LSCC cells due to the oxidative stress caused by ROS. Therefore, an MTT assay was performed to determine the cell viability of HN-3 LSCC cells following treatment with different doses of CBDCA. Subsequently, the expression levels of ROS and the rate of apoptosisecrosis were evaluated in the cells. Following this, the HN-3 cells were co-treated with CBDCA and glutathione (GSH) or H2O2, followed by an MTT assay, a cell migration assay and western blot analysis. The results demonstrated that CBDCA reduced the viability of HN-3 cells in a time- and dose-dependent manner and promoted the production of ROS and apoptosis at certain doses. Additionally, the combination treatment of CBDCA and H2O2 enhanced the inhibitory effects of CBDCA on cell viability and migration ability, and promoted apoptosis in HN-3 cells; whereas the combined treatment of CBDCA and GSH exerted opposite effects. The results of the present study demonstrated that CBDCA promotes the apoptosis of HN-3 cells through accumulation of ROS, which may provide a novel treatment strategy for treating LSCC.
机译:喉鳞状细胞癌(LSCC)目前在中国是一个严重的公共卫生问题。因此,迫切需要确定对该疾病的有效治疗策略。先前的研究表明,活性氧(ROS)在LSCC细胞凋亡中起重要作用。还已经表明,具有广泛抗肿瘤特性的第二代铂化合物卡铂(CBDCA)能够诱导氧化应激产生ROS,进而促进细胞凋亡。因此,本研究调查了CBDCA是否由于ROS引起的氧化应激而在LSCC细胞中具有细胞毒性。因此,在用不同剂量的CBDCA处理后,进行MTT测定以确定HN-3 LSCC细胞的细胞活力。随后,评估细胞中ROS的表达水平和细胞凋亡/坏死率。之后,将HN-3细胞与CBDCA和谷胱甘肽(GSH)或H2O2共同处理,然后进行MTT分析,细胞迁移分析和蛋白质印迹分析。结果表明,CBDCA以时间和剂量依赖性方式降低HN-3细胞的活力,并在一定剂量下促进ROS的产生和细胞凋亡。另外,CBDCA和H2O2的联合处理增强了CBDCA对细胞活力和迁移能力的抑制作用,并促进了HN-3细胞的凋亡。而CBDCA和GSH的联合治疗则产生相反的效果。本研究结果表明,CBDCA通过ROS的积累促进HN-3细胞的凋亡,这可能为治疗LSCC提供了一种新的治疗策略。

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