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. 2018 May 22;9(6):608. doi: 10.1038/s41419-018-0644-4

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© The Author(s) 2018

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 license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license 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 license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 7 — TRIM50 was significantly downregulated in HCC cells and its decreased expression further promoted HCC progression. Further investigation showed that TRIM50 could target SNAIL for K-48 linked poly-ubiquitous degradation and thus reversed SNAIL-mediated epithelial-to-mesenchymal transition (EMT) transition. Altogether, loss of TRIM50 in HCC cells led to upregulation of EMT process and further promoted the malignant behaviors of HCC cells, including proliferation, colony formation, anoikis resistance, and invasion, thus promoted HCC progression