Knockdown of Peroxiredoxin V increased the cytotoxicity of non-thermal plasma-treated culture medium to A549 cells

Hu-Nan Sun, Xiao-Yu Guo, Dan-Ping Xie, Xiao-Ming Wang, Chen-Xi Ren, Ying-Hao Han, Nan-Nan Yu, Yu-lan Huang, Taeho Kwon
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引用次数: 3

Abstract

Administration of non-thermal plasma therapy via the use of plasma-activated medium (PAM) might be a novel strategy for cancer treatment, as it induces apoptosis by increasing reactive oxygen species (ROS) levels. Peroxiredoxin V (PRDX5) scavenges ROS and reactive nitrogen species and is known to regulate several physiological and pathological reactions. However, its role in lung cancer cells exposed to PAM is unknown. Here, we investigated the effect of PRDX5 in PAM-treated A549 lung cancer cells and determined the mechanism underlying its cytotoxicity. Cell culture medium was treated with low temperature plasma at 16.4 kV for 0, 60, 120, or 180 s to develop PAM. PRDX5 was knocked down in A549 cells via transfection with short hairpin RNA targeting PRDX5. Colony formation and wound healing assays, flow cytometry, fluorescence microscopy, and western blotting were performed to detect the effect of PRDX5 knockdown on PAM-treated A549 cells. PAM showed higher cytotoxicity in lung cancer cells than in control cells, downregulated the mitogen-activated protein kinase signaling pathway, and induced apoptosis. PRDX5 knockdown significantly inhibited cell colony formation and migration, increased ROS accumulation, and reduced mitochondrial membrane potential in lung cancer cells. Hence, PRDX5 knockdown combined with PAM treatment represents an effective option for lung cancer treatment.
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过氧化氧还蛋白V的敲低增加了非热等离子体处理培养基对A549细胞的细胞毒性
通过使用等离子体活化介质(PAM)进行非热等离子体治疗可能是一种新的癌症治疗策略,因为它通过增加活性氧(ROS)水平来诱导细胞凋亡。过氧化氧还蛋白V (PRDX5)清除活性氧和活性氮,并调节多种生理和病理反应。然而,它在暴露于PAM的肺癌细胞中的作用尚不清楚。在这里,我们研究了PRDX5在pam处理的A549肺癌细胞中的作用,并确定了其细胞毒性的机制。用16.4 kV低温等离子体处理细胞培养基0、60、120、180 s,形成PAM。通过转染靶向PRDX5的短发夹RNA,在A549细胞中敲除PRDX5。通过菌落形成和伤口愈合实验、流式细胞术、荧光显微镜和western blotting检测PRDX5敲低对pam处理的A549细胞的影响。PAM对肺癌细胞的细胞毒性高于对照细胞,下调丝裂原激活的蛋白激酶信号通路,诱导细胞凋亡。PRDX5敲低显著抑制肺癌细胞集落形成和迁移,增加ROS积累,降低线粒体膜电位。因此,PRDX5敲除联合PAM治疗是肺癌治疗的有效选择。
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