IL-17 induces the proliferation and migration of glioma cells through the activation of PI3K/Akt1/NF-κB-p65
IL-17 induces the proliferation and migration of glioma cells through the activation of PI3K/Akt1/NF-κB-p65
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IL-17通过激活PI3K/Akt1/NF-kappa B-p65诱导胶质瘤细胞增殖和迁移
DOI：
10.1016/j.canlet.2019.01.008
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发表时间：
2019-01-01
期刊：
影响因子：
9.7
通讯作者：
Shi, Lei
中科院分区：
文献类型：
--
作者：
Wang, Bin;Zhao, Chen-Hui;Shi, Lei
白介素17(IL-17)作为一种促炎细胞因子，在胶质瘤患者血清和肿瘤组织中表达上调，但其对胶质瘤增殖和迁移的影响尚不清楚。本研究旨在探讨IL-17在胶质瘤细胞增殖和迁移中的作用及其可能机制。结果表明，IL-17不仅能促进体外培养的胶质瘤细胞的增殖和迁移，而且在体内也能促进BALB/c裸鼠胶质瘤细胞的成瘤。机制研究发现，IL-17刺激可增加胶质瘤细胞Akt1和NF-kappa B-p65的磷酸化水平，而PI3K、Akt1和NF-kappa B-p65的下调或抑制也可降低IL-17诱导的胶质瘤细胞的增殖和迁移。此外，PI3K/Akt1是IL-17孵育的胶质瘤细胞中NF-kappa B-p65激活的上游调节因子。此外，PI3K、Akt1和NF-kappa B-p65的抑制显著抑制了IL-17诱导的胶质瘤细胞的肿瘤形成。综上所述，IL-17可通过激活PI3K/Akt1/NF-kappa B-p65促进胶质瘤细胞的增殖和迁移，这些发现可能为脑胶质瘤的发病机制提供新的视角。
Interleukin 17 (IL-17), as a pro-inflammatory cytokine, is up-regulated in the sera and tumor tissues of glioma patients; however the effects of IL-17 on glioma proliferation and migration remain unclear. In this study, the roles of IL-17 in the proliferation and migration of glioma cells and their potential mechanisms were determined. The results showed that IL-17 could not only enhance the proliferation and migration of cultured glioma cells (in vitro), but also promote the tumor formation of glioma cells in BALB/c nude mice (in vivo). Mechanical exploration revealed that IL-17 stimulation could increase the phosphorylation levels of Akt1 and NF-kappa B-p65 in glioma cells, and knockdown or inhibition of PI3K, Akt1 and NF-kappa B-p65 could also reduce the IL-17-induced proliferation and migration of the glioma cells. Moreover, PI3K/Akt1 was the upstream regulator of NF-kappa B-p65 activation in IL-17-incubated glioma cells. Furthermore, the inhibition of PI3K, Akt1 and NF-kappa B-p65 markedly suppressed the tumor formation of glioma cells induced by IL-17. Together, these data indicate that IL-17 can promote the proliferation and migration of glioma cells via PI3K/Akt1/NF-kappa B-p65 activation, and these findings might provide a new insight into glioma pathogenesis.