PDF(Pubmed)
Abstract：
The therapeutic potential of cold physical gas plasma operated at atmospheric pressure in oncology has been thoroughly demonstrated in numerous preclinical studies. The cytotoxic effect on malignant cells has been attributed mainly to biologically active plasma-generated compounds, namely, reactive oxygen and nitrogen species. The intracellular accumulation of reactive oxygen and nitrogen species interferes strongly with the antioxidant defense system of malignant cells, activating multiple signaling cascades and inevitably leading to oxidative stress-induced cell death. This study aims to determine whether plasma-induced cancer cell death operates through a universal molecular mechanism that is independent of the cancer cell type. Using whole transcriptome data, we sought to investigate the activation mechanism of plasma-treated samples in patient-derived prostate cell cultures, melanoma, breast, lymphoma, and lung cancer cells. The results from the standardized single-cohort gene expression analysis and parallel multi-cohort meta-analysis strongly indicate that plasma treatment globally induces cancer cell death through immune-mediated mechanisms, such as interleukin signaling, Toll-like receptor cascades, and MyD88 activation leading to pro-inflammatory cytokine release and tumor antigen presentation.
摘要：
在肿瘤学中在大气压下操作的冷物理气体等离子体的治疗潜力已在许多临床前研究中得到充分证明。对恶性细胞的细胞毒性作用主要归因于生物活性血浆产生的化合物，即,活性氧和氮。细胞内活性氧和氮的积累强烈干扰恶性细胞的抗氧化防御系统，激活多个信号级联，不可避免地导致氧化应激诱导的细胞死亡。这项研究旨在确定血浆诱导的癌细胞死亡是否通过与癌细胞类型无关的通用分子机制起作用。使用整个转录组数据，我们试图研究患者来源的前列腺细胞培养物中血浆处理样品的活化机制,黑色素瘤，乳房,淋巴瘤和肺癌细胞。标准化单队列基因表达分析和平行多队列荟萃分析的结果强烈表明，血浆治疗通过免疫介导的机制在全球范围内诱导癌细胞死亡。如白细胞介素信号，Toll样受体级联,和MyD88激活导致促炎细胞因子释放和肿瘤抗原呈递。
