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. 2021 Mar 5;19:98. doi: 10.1186/s12967-021-02770-0

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© The Author(s) 2021

Open AccessThis 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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 3 — HPSE2, which was regulated by promoter DNA methylation, could be an independent prognostic factor. a Methylation levels of HPSE2 in 22 cases of CRC tissues in GSE17648; b Methylation levels of HPSE2 in 26 cases of matched CRC tumors and adjacent normal tissues in GSE29490; HPSE2 expression (c) and methylation (d) in TCGA database; e, f Kaplan–Meier curves showing that hypermethylation–low expression of HPSE2 was associated with the shortened survival of CRC patients at the late stages (f) but not at the early stages (e); g Univariate and multivariate COX regression model revealed that HPSE2 could be an independent prognostic risk factor. ***P < 0.001