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. 2020 Jun 23;39:118. doi: 10.1186/s13046-020-01617-8

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© The Author(s) 2020

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. 6 — Dysregulation of the TRIM25-SP1-MMP2 axis in GC. a-c Kaplan–Meier Overall Survival curves of human GC patients with low versus high TRIM25 (a), combined with TRIM25/SP1 (b) and combined with TRIM25/MMP2 (c) expressions, based on TCGA data (http://www.oncolnc.org/). d-e Protein levels of TRIM25 and SP1 were detected in GC tumor tissues and normal tissues by IHC. f The correlations of the TRIM25 protein levels and SP1 protein levels were calculated (n = 90). g-h Kaplan-Meier curves depicting OS according to the expression patterns of TRIM25 (g) and SP1 (h) in the GC cohort. P values were calculated with the log-rank test. i A working model of JP3 on inhibiting tumor angiogenesis of CC via activating TRIM25 signaling pathway