Department of Neurosurgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, 1277 Jiefang Avenue, Wuhan, Hubei 430022, China.
Department of Critical Care Medicine, People's Hospital of Dongxihu District, Wuhan, Hubei 430040, China.
Cell Signal. 2023 Aug;108:110731. doi: 10.1016/j.cellsig.2023.110731. Epub 2023 May 26.
A large amount of clinical and experimental evidence indicates that M1 macrophages can inhibit tumor progression and expansion; however, the molecular mechanism by which macrophage-derived exosomes inhibit the proliferation of glioblastoma cells has not yet been elucidated. Here, we used M1 macrophage exosomes encapsulating microRNAs to inhibit the proliferation of glioma cells. Exosomes derived from M1 macrophages exhibited high expression levels of miR-150, and the inhibition of glioma cell proliferation mediated by exosomes derived from M1 macrophages was dependent on this microRNA. Mechanistically, miR-150 is transferred to glioblastoma cells through M1 macrophages and binds to MMP16, downregulating its expression and inhibiting glioma progression. Overall, these findings indicate that M1 macrophage-derived exosomes carrying miR-150 inhibit the proliferation of glioblastoma cells through targeted binding to MMP16. This dynamic mutual influence between glioblastoma cells and M1 macrophages provides new opportunities for the treatment of glioma.
大量临床和实验证据表明，M1 巨噬细胞可以抑制肿瘤的进展和扩张；然而，巨噬细胞来源的外体抑制神经胶质瘤细胞增殖的分子机制尚不清楚。在这里，我们使用包裹 microRNA 的 M1 巨噬细胞外体来抑制神经胶质瘤细胞的增殖。M1 巨噬细胞衍生的外体表现出高表达 miR-150 的水平，并且 M1 巨噬细胞衍生的外体介导的神经胶质瘤细胞增殖抑制依赖于这种 microRNA。从机制上讲，miR-150 通过 M1 巨噬细胞转移到神经胶质瘤细胞中，并与 MMP16 结合，下调其表达并抑制神经胶质瘤的进展。总的来说，这些发现表明，M1 巨噬细胞衍生的携带 miR-150 的外体通过与 MMP16 的靶向结合抑制神经胶质瘤细胞的增殖。神经胶质瘤细胞和 M1 巨噬细胞之间的这种动态相互影响为治疗神经胶质瘤提供了新的机会。
