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. 2019 Oct 14;10(10):784. doi: 10.1038/s41419-019-2023-1

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© The Author(s) 2019

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. 1 — a The binding site of miR-3163 in the 3′-UTR of ADAM-17. The bold and italicized fonts indicate the wild-type or mutant forms of putative miR-3163 targeting sequences. b The relationship between the expression level of miR-3163 and ADAM-17 in advanced HCC specimens was assessed through the Spearman’s rank correlation analysis. c A total of 52 patients were divided into two groups (ADAM-17-high group or ADAM-17-low group) according to the median value of ADAM-17 expression. d, e Kaplan–Meier survival curves and log-rank tests were used to analyze the OS (d) or TTP (e) in advanced HCC patients with low or high levels of ADAM-17, who received treatment with sorafenib. f A total of 52 patients were divided into two groups (miR-3163-high group or miR-3163-low group) according to the median value of miR-3163 expression. g, h Kaplan–Meier survival curves and log-rank tests were used to analyze the OS (g) or TTP (h) in advanced HCC patients with low or high levels of miR-3163, who received treatment with sorafenib. *P < 0.05