AI Article Synopsis
- Interleukin 17 (IL-17) is a cytokine that is elevated in glioma patients, but its specific effects on glioma cell growth and movement were not well understood before this study.
- The study found that IL-17 boosts both the growth and movement of glioma cells in laboratory settings and enhances tumor formation in mouse models.
- Mechanistically, IL-17 activates signaling pathways involving PI3K, Akt1, and NF-κB-p65, and inhibiting these pathways can reduce the stimulating effects of IL-17 on glioma cells.
Article Abstract
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-κB-p65 in glioma cells, and knockdown or inhibition of PI3K, Akt1 and NF-κB-p65 could also reduce the IL-17-induced proliferation and migration of the glioma cells. Moreover, PI3K/Akt1 was the upstream regulator of NF-κB-p65 activation in IL-17-incubated glioma cells. Furthermore, the inhibition of PI3K, Akt1 and NF-κB-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-κB-p65 activation, and these findings might provide a new insight into glioma pathogenesis.
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| http://dx.doi.org/10.1016/j.canlet.2019.01.008 | DOI Listing |
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