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. 2019 Nov 29;4:51. doi: 10.1038/s41392-019-0086-1

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© The Author(s) 2019

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 license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license 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 license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 8 — A model showing the role of HOXB13 in RCC. HOXB13 is downregulated in RCC tumor tissue compared to normal tissue and LCC tumor tissue. HOXB13 downregulation in RCC is caused by the DNMT3B-induced methylation of an upstream CpG island, which increases C-myc expression by activating the β-catenin/TCF4 complex, thus enhancing tumor cell proliferation and migration