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. 2018 Jul 6;9:1557. doi: 10.3389/fimmu.2018.01557

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Copyright © 2018 Zhang, Feng, Fu, Liu, Yu, Sun, She, Li, Zhao, Liu, Liu, Liu, Liu, Li and Wu.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Schematic model of the molecular mechanisms representing the function of factor X (FX) in glioblastoma multiforme (GBM) tumor growth. FX secreted by GBM cells to the tumor microenvironment and recruited macrophages to the tumor via interactions with CD11b on the surfaces of macrophages. FX phosphorylated and activated extracellular signal-related kinase (ERK)1/2 and AKT in macrophages, leading to M2 subtype macrophage polarization, which facilitated GBM tumor growth. In GBM cells, miR-338-3p and lncRNA CASC2c inhibited the expression of FX. lncRNA CASC2c also interacted with miR-338-3p and reciprocally repressed it. FX interacted with ERK1/2 and decreased p-ERK1/2.