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. 2023 Jun 23;22:99. doi: 10.1186/s12943-023-01791-1

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© The Author(s) 2023

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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 5 — Overexpression of IGF2BP2 in endothelial cells activates the PI3K-Akt signaling to promote angiogenesis. A Circle diagram showing the relationships between LUAD_IGF2BP2 ligand genes and En_IGF2BP2 receptor genes. The gene colors characterize their logFC and the pathway colors are aligned with the circles. The first loop genes are shared markers for the LUAD_IGF2BP2 and the En_IGF2BP2 subpopulations, the second loop is a non-shared marker, and the third and fourth loops are signaling pathways. B Violin diagram showing the expression pattern of exosomal markers in the LUAD subpopulations. C Pathway map showing the PI3K-Akt signaling pathway activated in the En_IGF2BP2 subpopulation