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. 2021 Oct 26;13(10):1417–1445. doi: 10.4252/wjsc.v13.i10.1417

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©The Author(s) 2021. Published by Baishideng Publishing Group Inc. All rights reserved.

This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/Licenses/by-nc/4.0/

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Schematic illustration of the involvement of SOX2 and SOX9 in the chemoresistance and radioresistance of glioma stem cells. The expression of stemness-related transcription factor SOX2 is elevated in glioma stem cells (GSCs) through various mechanisms (decreased expression of miR-145 and miR-9* that directly target SOX2, direct transcriptional activation by Forkhead box M1 and through mammalian target of rapamycin signaling) contributing to chemo- and radioresistance of GSCs. SOX2 directly activates the expression of ABCC3 and ABCC6 transporters. mTOR signaling affects the SOX2/SOX9 axis, contributing to chemoresistance. The ERK1/2/miR-124/SOX9 axis and direct targeting of PDK1 (pyruvate dehydrogenase kinase 1) by SOX9 have a role in resistance to radiation and temozolomide, respectively. References are included in the main text. GSCs: Glioma stem cells; FOXM1: Forkhead box M1; mTOR: Mammalian target of rapamycin; PDK1: Pyruvate dehydrogenase kinase 1.