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. 2018 Feb 23;7(2):22. doi: 10.1038/s41389-017-0010-x

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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. 4 — a Putative and mutant binding sites of miR-HCC1 on 3’UTR of NFIX. b Fluorescent reporter assay was conducted 48 h after transfection with pri-miR-HCC1 or ASO-miR-HCC1 in Huh7 and HepG2 cells. c mRNA and protein levels of NFIX at 48 h after transfection with miR-HCC1 or empty vector. d mRNA levels of NFIX in HCC tissues and adjacent noncancerous tissues were evaluated by RT-qPCR (n = 20). e Pearson’s correlation analysis between miR-HCC1 and NFIX expression in HCC tissues. All data were compared with the corresponding control groups. The data are shown as the mean ± SD (*P < 0.05; **P < 0.01; ns not significant)