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. 2021 Apr 12;40(18):3318–3330. doi: 10.1038/s41388-021-01765-x

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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. 6 — A The expression levels of PTEN, AKT, p-AKT, p21, and p27 were detected by Western blots in the PTEN-silenced HeLa-PRDM4 and SiHa-PRDM4 cells. B, C PTEN was silenced by specific shRNA targeting the PTEN CDS region in the PRDM4-overexpressing HeLa and SiHa cells, and the associated tumor weights and growth curves are shown. D The expression levels of AKT and p-AKT were detected in the HeLa-PRDM4 and SiHa-PRDM4 cells treated with the PTEN inhibitor SF1670. E The cell proliferation and cell vitality were assessed in the HeLa-PRDM4 and SiHa-PRDM4 cells treated with the PTEN inhibitor SF1670. F The correlation between the PRDM4 and PTEN mRNA levels in cervical cancer was analyzed using the TCGA database (R = 0.24, p < 0.05). G A proposed model of the PRDM4-mediated enhancement of PTEN inactivation of the PI3K/AKT pathway in cervical cancer progression. The data are presented as the mean ± SD of experiments in triplicate. Statistical significance is denoted by the symbols *p < 0.05, **p < 0.01, ***p < 0.001.