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. 2020 Apr 18;2(1):vdaa047. doi: 10.1093/noajnl/vdaa047

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© The Author(s) 2020. Published by Oxford University Press, the Society for Neuro-Oncology and the European Association of Neuro-Oncology.

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact journals.permissions@oup.com

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Figure 1. — An inflammatory microenvironment induces proinflammatory gene expression in GBM cells. Immuno-miR-93 is repressed in GBM. (A) mRNA expression of inflammatory genes in U87 (left panel, n = 3) and T98G (middle panel, n = 5) cells after stimulation with either IL-1β or supernatant of stimulated PBMCs (right panel, n = 3). (B) Protein expression of inflammatory genes after stimulation with IL-1β in U87 (left panel, n = 3) and T98G (right panel, n = 3) cells. All experiments were performed in triplicates; *P < .05; **P < .01. (C) Normalized expression levels of miR-93 in GBM biopsies (n = 51), primary GBM cell lines (n = 8), U87, T98G cells (n = 6), and normal brain tissue (n = 9). Endogenous reference: U47; *P < .05.