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. 2021 Jan 21;12(1):105. doi: 10.1038/s41419-021-03411-6

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© The Author(s) 2021

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 — In cervical cancer, loss of HOXB4 upregulated β-catenin and its downstream gene c-Myc, which contributed to the enhancement of the cell cycle and promoted tumor progression. In HOXB4-overexpressing cervical cancer cells, HOXB4 was accessed to the nucleus and transcriptionally repressed β-catenin expression, leading to impaired nuclear accumulation of β-catenin, which subsequently contributed to the inhibition of tumor progression.