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. 2020 Jun 4;11(6):420. doi: 10.1038/s41419-020-2629-3

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© The Author(s) 2020

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 — The expression of TP53 in HOXA5-modified cervical cancer cells was determined by real-time PCR (a) and western blot (b). The expression of p53 in xenograft was determined by IHC (c). d–f The expression of HOXA5, p53, and p21 in clinical cervical cancer specimens was determined by western blot and the correlation was analyzed. g HOXA5 expression was significantly positively correlated with the expression of p53 (r = 0.4118, p < 0.001) in cervical cancers (data from GEO database). h, i The TP53 promoter structure was constructed and luciferase activity relative to Renilla control was measured in HeLa-HOXA5 and SiHa-HOXA5 cells. j The qChIP assay is shown in HeLa-HOXA5 and SiHa-HOXA5 cells immunoprecipitation by HOXA5 antibody and IgG antibody (as the negative control). k An experimentally defined transcription factor binding sites of HOXA5 was found in the JASPAR CORE database. The data were shown as the mean ± SD of three independent experiments. *p < 0.05, **p < 0.01, ***p < 0.001.