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. 2021 Jun 21;40:200. doi: 10.1186/s13046-021-01994-8

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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. 6 — Expression of IMP3 and MEKK1/MEK/ERK in clinical CRC samples. (A) Representative images and the number of IMP3, MEKK1, MEK1 and p-ERK detected by IHC in CRC tissue microarrays. (B) IMP3, MEKK1, MEK1 and p-ERK expression in adjacent normal colon mucosa (n = 114, up panel) and colorectal cancer tissue (n = 282, lower panel). (C)Correlation of IMP3 expression with MEKK1, MEK1 and p-ERK. (D) KaplaneMeier analyses for the FUSCC dataset. Patients were divided into three groups based on the expression of IMP3 and MEKK1 (negative or positive). Both positive groups had the poorest prognosis with the lowest DFS and OS. (E)Schematic model showing the role of IMP3 in regulating MEKK1/MEK1/ERK Signaling Pathway in the Progression of Colorectal Cancer