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. 2023 Nov 27;18:80. doi: 10.1186/s13062-023-00439-w

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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. 6 — RCC2 drives tumor development by promoting Gli1 in vivo. A Figs of mouse xenograft tumors from the Ctrl, RCC2 overexpression, and RCC2 overexpression + GANT61 groups. B Tumor growth curves in mice among three groups. C Tumor weight of mice among three groups. D The protein expression of RCC2, Gli1, SOX2, Nanog, and CD44 in mice among three groups were tested with western blot. *P＜0.05, **P＜0.01, ***P＜0.001