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. 2018 Sep 20;9(10):954. doi: 10.1038/s41419-018-0978-y

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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 The mRNA levels of PTPRB in 50 paired human HCC and adjacent normal tissues. b The mRNA levels of PTPRB expression in HCC cell lines and normal L02 cells. c Representative immunostaining images of PTPRB in HCC tissues and adjacent normal tissues. d A negative correlation between the levels of miR-665 and PTPRB expression in HCC specimens. e The mRNA level of PTPRB expression in overexpressing or silencing miR-665 HepG2 and SMMC7721 cells; cells transfected with empty lentiviral vectors were used as a negative control. f The protein levels of PTPRB in overexpressing or silencing miR-665 HepG2 and SMMC7721 cells; cells transfected with empty lentiviral vectors were used as a negative control. g The potential miR-665 binding site in the PTPRB 3′-UTR was predicted by TargetScan. h Dual-luciferase reporter assay was used to analyze the effects of miR-665 expression on the activities of WT and MUT PTPRB 3′-UTR. All data are represented as the means ± SD. ^* P < 0.05, ^** P < 0.01, ^*** P < 0.001