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. 2020 May 5;39(23):4538–4550. doi: 10.1038/s41388-020-1307-3

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© The Author(s) 2020

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. 3 — a The correlation between LINC01278 gene expression and miR-1258 level in TCGA dataset. b The correlation between LINC01278 gene expression and miR-1258 level in SYSUCC dataset. c The expression of miR-1258 in HCC cells transfected by LINC01278 and shLINC01278. d LINC01278 is abundant in cytoplasm of SMMC-7721 and Hep3B cells. U2 and actin were used as positive control. e Cytoplasm enrichment of LINC01278 in HCC patients’ tissues. f The predicted binding sites between miR-1258 and LINC01278. The muted site (LINC01278-mut) was used for luciferase reporter assay. The relative luciferase activities were detected in 293 T cells transfected by LINC01278-WT and LINC01278-mut. g RNA-IP was used to identify the inhibition of miR-1258 by LINC01278. The expression levels of LINC01278 and miR-1258 were detected using qRT-PCR. LINC01278, ectopic LINC01278 expression in HCC cells. shLINC01278, HCC cells were transfected by shRNA target LINC01278. *P < 0.05.