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. 2022 Jun 7;20:262. doi: 10.1186/s12967-022-03467-8

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© The Author(s) 2022

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. 8 — Stress-induced CEBPB is the upstream transcription factor of TRIM2. A The Venn diagram shows the overlap of the upstream transcription factor of TRIM2 predicted by PROMO (a) and the gene regulated by EPI detected by transcriptome sequencing (b). B–D Immunoblot and qPCR analysis indicated that the expression of CEBPB is regulated by EPI. E Immunoblot analysis indicated that the expression of TRIM2 is regulated by CEBPB. F–H ChIP assays with CEBPB antibody or IgG were performed to verify binding between CEBPB and the TRIM2 promoter in 293 T cells. I-J Transwell assays revealed that CEBPB promotes migration in CRC cells. K Colony formation assays revealed that CEBPB promotes proliferation in CRC cells. L-M Western blot analysis indicated that inhibiting CEBPB expression reverses the EPI-induced promotion of EMT and CSCs in CRC cells. *P < 0.05, **P < 0.01, ***P < 0.001