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. 2023 Nov 9;21:319. doi: 10.1186/s12964-023-01320-z

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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. 8 — Hypothetic schematic model of response to USP7 inhibition and therapeutic benefits of targeting both USP7 and USP22 in human cancer. Upregulation of USP22 upon USP7 inhibition may activate downstream signaling pathways of USP22 such as c-Myc and H2Bub1 as well as FOXP3 (data not shown) and PD-L1 (data not shown) in cancer cells, which may antagonize antitumor activity of USP7 in human cancer cells, while targeting both USP7 and USP22 will induce broad and synergistic anti-cancer effects