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. 2020 Feb 13;9(2):19. doi: 10.1038/s41389-020-0207-2

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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. 5 — a Analysis using TargetScan, miRanda, and miRDB revealed that several miRNAs might regulate GLUT1. b The miR-148a mRNA level was analyzed in 28 iCCA and paracancerous specimens using qRT-PCR. c Kaplan–Meier survival analyses were conducted to assess the influence of miR-148a on overall survival. d The binding site of miR-148a in the wild-type (WT) 3′-untranslated region (UTR) of GLUT1 and the corresponding mutant type were constructed. e A luciferase assay of GLUT1 3′-UTR and GLUT1 3′-UTR-mut reporters cotransfected with a miR-148a mimic or miR-148a inhibitor in the indicated cells. f MiR-148a overexpression or silencing decreased or increased GLUT1 mRNA in the indicated cells. g Correlation analysis indicated an inverse correlation between miR-148a and GLUT1 expression. Data are means ± SD of three independent experiments. *P < 0.05; **P < 0.01; ***P < 0.001.