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. 2022 Jul 5;24(3):294. doi: 10.3892/ol.2022.13414

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Copyright: © Wang et al.

This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

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Figure 2. — Related homolog genes (e.g. QKI), transcription factors (e.g. NANOG) and sialidase (e.g. NEU4) are able to activate the HH signaling pathway to maintain the self-renewal ability of GSCs by increasing SHH/GLI1 expression. ID1 and DLG5 inhibit cullin-3 ubiquitin ligase, activate HH signaling and promote GSC proliferation and tumorigenicity. DRP5 is specifically upregulated in the proneural subtype of GSC. NS activates the Wnt and HH signaling pathways by regulating the β/AKT axis of β-catenin and Gli1, respectively. Vascular endothelial cells in the tumor microenvironment may provide SHH to further activate HH signaling pathways, thereby promoting GSC properties. QKI, Quaking homolog; DRP5, dihydro pyrimidine-associated protein 5; SHH, Sonic Hedgehog; GBM, glioblastoma; SMO, smoothened; Gli, glioma-associated oncogene; GSC, glioblastoma stem cells; ID1, differentiation inhibitor 1; NS, microenvironmental nutritional stress; DLG5, discs large homolog 5.