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. 2023 Sep 7;22:148. doi: 10.1186/s12943-023-01843-6

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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 — The function of NETs in the TME. Tumor cells possess the ability to secrete various molecules, including G-CSF and NAMPT. G-CSF can induce the formation of NETs, which exhibit diverse biomedical behaviors such as epithelial-to-mesenchymal transition, capture of CTCs, and increased vascular permeability that contribute to tumor prognosis [133]. However, they can also exhibit laminin remodeling and immunosuppressive behaviors that promote tumor metastasis [133]. On the other hand, NAMPT can stimulate the formation of aged neutrophil-derived NETs with high CXCR4 expression and low CD62L expression, consequently promoting tumor metastasis [137]