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. 2023 Dec 12;21:909. doi: 10.1186/s12967-023-04616-3

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© The Author(s) 2023

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 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. 5 — Relationship of SPOCK1 with methylation and mutation. Boxplot indicates the extent of variation in promoter methylation levels in LUAD samples from the UALCAN database, (A) in normal and tumor, (B) TP53 mutant and TP53 wild-type groups. C Exploration of the mutational landscape of SPOCK1 in LUAD using the cBioPortal database. Mutation waterfall plots of the top 20 genes in the (D) high SPCOK1 group and (E) low SPCOK1 group in terms of mutation frequency. F Boxplots show the difference of DNA damage measures between different levels of SPOCK1 expression groups (Wilcon rank-sum test). (***p < 0.001; **p < 0.01; *p < 0.05; ns. no significance.)