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. 2021 Jun 15;12(6):615. doi: 10.1038/s41419-021-03882-7

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© The Author(s) 2021

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 8 — Prrx1 plays a critical role in regulating glioma stemness and angiogenesis. On the one hand, Prrx1 upregulated TGF-β1 expression by directly binding to the promoter region as a transcription factor. The autocrine TGF-β1 activates the TGF-β/smad pathway, upregulates the stemness and proangiogenic related genes, and consequently promotes stemness and angiogenesis in glioma. On the other hand, the paracrine TGF-β1 as well as other proangiogenic factors like VEGF act on the endothelial cells, promote their migration and tube formation ability and consequently stimulate the formation of glioma vessels.