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. 2018 Jan 24;9(2):92. doi: 10.1038/s41419-017-0134-0

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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. 2 — a The putative miR-375 binding sites in the 3’UTR of YAP1, TEAD4, and CTGF as predicted by www.microrna.org and www.targetscan.org. b mRNA expression of YAP1, TEAD4, and CTGF after miR-375 transfection in AGS, NCI-N87, and MGC-803 cells (**, P < 0.001). c miR-375 ectopic expression decreased YAP1, TEAD4, and CTGF protein expression in AGS, NCI-N87, and MGC-803 cells. d miR-375 suppressed the relative luciferase activity in the constructs which contain the wild type sequence of the binding site in the 3’UTR of YAP1 (only binding site 2), TEAD4, and CTGF (*, P < 0.05; **, P < 0.001). Wild type, luciferase construct containing wild type binding site in YAP1 3’UTR; Mutation, mutated nucleotides were introduced to the complementary seed sequence. e YAP1 and CTGF protein expression showed negative correlation with miR-375 expression in primary gastric tumors (n = 28, P < 0.001 and P = 0.044, respectively)