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. 2023 Nov 18;22:184. doi: 10.1186/s12943-023-01871-2

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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. 5 — DNMTs promote hypermethylation of ELF5 in RCC. (A) UALCAN database was utilized to predict ELF5 methylation status in KIRC samples and normal samples. (B) MSP assay was utilized to detect ELF5 methylation in HK-2, 769-P, and A498. (C) UALCAN database was utilized for predicting DNMT1, DNMT3A, and DNMT3B expression in KIRC. (D) The correlation between ELF5 and DNMT1/DNMT3A/DNMT3B in RCC patient tissues (n = 21). (E-F) ELF5 expression was determined by RT-qPCR and western blot in cells when DNMT1, DNMT3A, or DNMT3B was silenced. (G-H) ELF5 level was determined through RT-qPCR when DNMT1/DNMT3B was overexpressed, and 5-Aza‐dC was added in cells. Two-tailed Student’s t test was performed. The error bars represent SD. ns means no significance, ^***p < 0.001