Journal
CANCER LETTERS
Volume 447, Issue -, Pages 93-104Publisher
ELSEVIER IRELAND LTD
DOI: 10.1016/j.canlet.2019.01.008
Keywords
Glioma; IL-17; PI3K/Akt1; NF-kappa B
Categories
Funding
- National Natural Science Foundation of China [81772691, 81000963, 81370062, 81201976, 81672499]
- China postdoctoral science foundation [2017M620196, 2018T110467]
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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.
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