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. 2022 Oct 19;11:75. doi: 10.1186/s40164-022-00322-w

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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.2 — TRIM family members are involved in cancer development. TRIM family members are involved in cancer development through mediating the abnormal cellular signaling pathway transduction including JAK/STAT, PI3K/AKT, TGF-β, Wnt/β-catenin, NF-κB, p53 hub, and other signaling pathways such as Notch, MAPK, AMPK, YAP. TRIMs affect upstream factors and downstream effectors through positive regulations and negative regulations which are mainly achieved by exerting their E3 ligase activity and promoting the ubiquitination degradation of target proteins. By interfering these crucial signaling pathways, TRIMs influence proliferation, migration, and invasion characteristics of cancer cells