Plasma-activated medium triggers cell death and the presentation of immune activating danger signals in melanoma and pancreatic cancer cells

Plasma-activated medium triggers cell death and the presentation of immune activating danger signals in melanoma and pancreatic cancer cells
复制标题

DOI:
10.1038/s41598-019-40637-z
复制
发表时间:
2019-03-11
期刊:
影响因子:
4.6
通讯作者:
Sardella, Eloisa
Sardella, Eloisa
中科院分区:
综合性期刊3区
文献类型:
--
作者:
Azzariti, Amalie;Iacobazzi, Rosa Maria;Sardella, Eloisa

文献摘要

被引文献

相似文献

在过去的十年中,冷大气等离子体在癌症治疗中显示出有前途的应用。血浆激活介质的治疗用途是在称为血浆药学的新兴领域中解决的主题。在肿瘤学中,等离子体活化介质用于在氧化剂与癌细胞接触时利用氧化剂的治疗作用。在血浆激活的液体培养基(PALM)的抗癌作用的几个因素中,H2O2和NO衍生物可能在凋亡途径中起关键作用。尽管近年来产生了大量的文献,但对PALM发挥其抗癌细胞活性的机制的充分理解是有限的。本文利用密封介质阻挡放电研究了活性氮和活性氧对癌细胞的作用。已经研究了两种以不良预后为特征的癌症:转移性黑色素瘤和胰腺癌。暴露于富含H2O2的PALM的两种肿瘤模型均显示增殖减少和钙网蛋白暴露和ATP释放增加,表明活化培养基通过激活先天免疫系统作为免疫原性细胞死亡诱导剂的潜在用途。
Over the past decade, cold atmospheric plasmas have shown promising application in cancer therapy. The therapeutic use of plasma-activated media is a topic addressed in an emerging field known as plasma pharmacy. In oncology, plasma-activated media are used to harness the therapeutic effects of oxidant species when they come in contact with cancer cells. Among several factors that contribute to the anticancer effect of plasma-activated liquid media (PALM), H2O2 and NO derivatives likely play a key role in the apoptotic pathway. Despite the significant amount of literature produced in recent years, a full understanding of the mechanisms by which PALM exert their activity against cancer cells is limited. In this paper, a sealed dielectric-barrier discharge was used to disentangle the effect of reactive nitrogen species (RNS) from that of reactive oxygen species (ROS) on cancer cells. Two cancers characterized by poor prognosis have been investigated: metastatic melanoma and pancreatic cancer. Both tumour models exposed to PALM rich in H2O2 showed a reduction in proliferation and an increase in calreticulin exposure and ATP release, suggesting the potential use of activated media as an inducer of immunogenic cell death via activation of the innate immune system.