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. 2020 Sep 25;20:465. doi: 10.1186/s12935-020-01493-4

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© The Author(s) 2020

Open AccessThis 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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 6 — HERPUD1 is directly targeted by miR-370. a miR-370 binding sites on HERPUD1 predicted by TargetScan. b Target relationship between miR-370 and HERPUD1 determine by dual luciferase assay. c RT-qPCR determining HERPUD1 expression in gastric cancer and adjacent normal tissues (N = 87). d Correlation between miR-370 and HERPUD1 in tissues. e HERPUD1 expression in normal gastric epithelial cells and gastric cancer cell lines determined by RT-qPCR. *p < 0.05 vs. adjacent normal tissues or mimic NC. ^#p < 0.05 vs. inhibitor NC. Data were shown as the mean ± standard deviation. When two paired group data followed normal distribution and homogeneity of variance, statistical comparison was performed with paired t-test. Two unpaired group which followed normal distribution and homogeneity of variance was analyzed by unpaired t-test. The experiment was repeated in triplicate