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. 2024 Dec 21;14:153. doi: 10.1186/s13578-024-01333-2

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© The Author(s) 2024

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. 4 — UHRF1 underlies SIRT6-deficiency-mediated BLCA progression. A Differential analysis of UHRF1 levels in normal and tumor samples from TCGA-BLCA cohort. B 253J cells were transfected with shUHRF1#1 and shScramble, and expressions of UHRF1 were detected with western blotting and RT-qPCR assays. C CCK-8 assay showed that cell viability was decreased in 253J and HT-1376 cells. D-E CCK-8 assay and colony formation assay revealed that cell viability was decreased in SIRT6-KD T24 and UMUC-3 cells after UHRF1 knockdown. F Indicated UMUC-3 cells were subcutaneously injected into BALB/c nude mice. Immunohistochemical detection of Ki-67 and CD34 in tumors derived from indicated cells were shown. G-H Quantification of tumor growth curve and tumor weights were compared among indicated tumors. *p < 0.05, **p < 0.01, ***p < 0.001, ns no significance