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. 2020 Dec 21;14:587747. doi: 10.3389/fncel.2020.587747

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Copyright © 2020 Zhuang, Chen, Cai, Wang, Yang, Li, Yang and Zhu.

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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FOXQ1 inhibition compensated the effect of miR-125b inhibition on cell apoptosis and neurite outgrowth. Comparisons of FOXQ1 expression (A,B), cell apoptosis (C,D), and neurite outgrowth (E,F) among blank, NC, inhibitor-miR, Si-FOXQ1, and inhibitor-miRandSi-FOXQ1 cells in primary neuron AD model. Comparisons of FOXQ1 expression (G,H), cell apoptosis (I,J), and neurite outgrowth (K,L) among blank, NC, inhibitor-miR, Si-FOXQ1, and inhibitor-miRandSi-FOXQ1 cells in PC-12 cellular AD model. MiR-125b, microRNA-125b; FOXQ1, forkhead box Q1; AD, Alzheimer disease; NC, negative control. *p < 0.05, **p < 0.01.