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. 2022 Jun 13;13(6):547. doi: 10.1038/s41419-022-04983-7

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© The Author(s) 2022

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. 7 — Schematic model showed regulation of KDM2A in human bladder cancer. KDM2A was frequently amplified and implicated in SEs formation in high-grade bladder cancer. Frequent upregulation of KDM2A was attributed to decreased H3K36me2 enrichment at tumor suppressor RARRES3, thus downregulating mRNA levels. The combination of IOX1 (KDM2A inhibitor) and ATRA (RARRES3 activator) can reverse this regulatory process.