胶质母细胞瘤（GBM）是一种最具侵袭性和挑战性的癌症之一。尽管对包括GBM在内的数十种癌细胞进行了广泛的研究，但冷等离子体（CAP）对GBM细胞的侵袭性迁移的影响却受到了有限的关注，而其潜在机制仍不明确。本研究旨在调查ns-CAPJ抑制人类GBM细胞侵袭性迁移的潜在分子机制。研究结果表明，ns-CAPJ显著降低了GBM细胞的侵袭和迁移，并诱导了GBM细胞的凋亡。进一步的机制研究显示，上皮间质转化（EMT）信号通路的抑制与ns-CAPJ对GBM细胞侵袭性迁移的抑制效应之间存在直接相关性。此外，结合N-乙酰半胱氨酸（NAC，ROS抑制剂）试验，我们发现ns-CAPJ刺激的ROS在抑制EMT过程中发挥了重要作用。这项工作有望为理解ns-CAPJ如何抑制人类GBM细胞的增殖和迁移提供新的见解。版权所有 © 2023. 由Elsevier Inc.发表。

Glioblastoma (GBM) is one of the most aggressive and challenging cancers to treat. Despite extensive research on dozens of cancer cells, including GBM, the effect of cold atmospheric plasma (CAP) on the invasive migration of GBM cells has received limited attention, and the underlying mechanisms remain poorly understood. This study aims to investigate the potential molecular mechanism of ns-CAPJ in inhibiting the invasive migration of human GBM cells. The findings indicate that ns-CAPJ significantly reduces GBM cell invasion and migration, and induces apoptosis in GBM cells. Further mechanistic studies demonstrate a direct correlation between the suppression of the epithelial-mesenchymal transition (EMT) signaling pathway and ns-CAPJ's inhibitory effect on GBM cell invasion and migration. Additionally, combined with the N-acetyl cysteine (NAC, a ROS inhibitor) assay, we found that the ROS stimulated by the ns-CAPJ plays an important role in suppressing the EMT process. This work is expected to provide new insight into understanding the molecular mechanisms of how ns-CAPJ inhibits the proliferation and migration of human GBM cells.Copyright © 2023. Published by Elsevier Inc.