芬太尼被广泛用于癌症患者的麻醉和镇痛。最近的研究揭示了它在几类癌症中的抗生长效应。胶质瘤是中枢神经系统最常见的原发性肿瘤，预后不良。为了探究芬太尼对胶质瘤的影响，使用不同浓度的芬太尼处理胶质瘤细胞在体内外进行研究，评估了增殖和侵袭表型及相关蛋白质的表达在两种人类胶质瘤细胞系(U251和U87)中。将阿片受体拮抗剂纳洛酮引入培养基以评估MOR在芬太尼介导的变化中的参与程度。与对照组相比，发现芬太尼只在高浓度下抑制胶质瘤细胞功能。Western blot和免疫荧光结果显示，芬太尼通过调节可能与MOR无关的NF-κB（P65）激活来发挥作用。此外，通过转染P65表达载体过表达P65恢复了芬太尼抑制的胶质瘤细胞的侵袭和迁移。总之，该研究显示阿片类镇痛药物芬太尼在高浓度下能够降低胶质瘤细胞的侵袭性，在体外和体内均有作用，可能通过调节P65激活来实现。版权所有©2023 Elsevier B.V.发布。

Fentanyl is widely used for anesthesia and analgesia in cancer patients. Recent studies have revealed its anti-growth effect in several categories of cancer. Gliomas are the most common primary tumors in the central nervous system with poor prognosis. To investigate the effects of fentanyl on gliomas, glioma cells were treated with different concentrations of fentanyl both in vitro and in vivo. Consequences of proliferation and invasive phenotypes, and related protein expression were evaluated in two human glioma cell lines (U251 and U87). Naloxone, Mu Opioid Receptor (MOR) antagonist, was introduced into culture media to assess the involvement of MOR in Fentanyl-mediated changes. When compared with control group, it could be found that Fentanyl inhibited function of glioma cells only at high concentrations. Western blot and immunofluorescence results revealed that Fentanyl exerted its action via modulating NF-κB (P65) activation which is likely independent of MOR . Moreover, overexpression of P65 by transfection P65-expressing vector restored the invasion and migration of glioma cells, which were inhibited by Fentanyl. In summary, this study showed that opioid pain medication Fentanyl was capable of decreasing invasiveness of glioma cells at a high concentration both in vitro and in vivo, likely via modulating P65 activation.Copyright © 2023. Published by Elsevier B.V.