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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. 7 — PD5091 induced more apoptosis and suppressed angiogenesis in USP22-Ko cancer cells. A. Multiplex IHC analysis of USP22 (Purple), Ki67 (Teal), and cleaved caspase-3 (Yellow) in the parental and USP22-Ko A549 xenograft tissues treated with P5091. B. Semi-quantitative analysis of Ki67-positive and cleaved caspase 3- positive cell populations in the parental and USP22-Ko A549 treated with P5091. C. IHC analysis of CD31 (Brown) in the parental and USP22-Ko A549 xenograft tissues treated with P5091 (Left panel), and semi-quantitative analysis of MVD in these xenografts (Right panel), *p<0.05, compared to Vehicle. D. IHC analysis of USP7 (Brown) in the parental and USP22-Ko A549 xenografts treated with P5091