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. 2022 Feb 2;7:33. doi: 10.1038/s41392-021-00855-2

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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. 7 — Analysis on transcriptomes of LN18^{PDGFRA−/−} treated with PBS, PDGFA or EFNA1. a Volcano graph of genes affected by PDGFA or EFNA1 vs. PBS. b Venn diagram of genes affected by PDGFA or EFNA1 vs. PBS. c Venn diagram of genesets enriched by PDGFA or EFNA1-upreguleted genes. d GSEA graph of EMT hallmark signature enriched by PDGFA or EFNA1-regulated genes. e Schematic diagram of EPHA2 and PDGFRA-mediated PDGFA function in GBM cells. Both PDGFRA and EPHA2 mediate PDGFA function to promote invasive growth and therapeutic resistance of GBM cells (upper panel). Single pharmaceutical inhibition of EPHA2 or PDGFRA cannot effectively suppress PDGFA activity due to the existence of compensate pathway. Concurrent inhibition of PDGFRA and EPHA2, however, potently block PDGFA signaling transduction (lower panels).