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. 2023 Apr 3;55(4):692–705. doi: 10.1038/s12276-023-00969-3

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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 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. 6 — a FDA-approved drugs as potential candidates for ECs that inhibit crosstalk between tumor cells and the TME; these candidates include tumor vasculature, ECM, and inflammatory factors. b Combining an IC and EC to enhance therapeutic responsiveness by blocking signaling crosstalk that converges to a cancer pathway. c Combining an IC and EC to overcome negative feedback in the MAPK signaling pathway. d Targeting tumor checkpoint modules. The epigenetic modulator DNA methyltransferase 1 (DNMT1) is downstream of multiple cancer-relevant pathways and promotes tumorigenesis. Targeting DNMT1 restores the normal activity downstream of multiple cancer-associated signaling pathways.