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. 2020 Sep 5;39:179. doi: 10.1186/s13046-020-01687-8

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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. 5 — STAT1 is a functional target of miR-382–3p and regulated by PSMB8-AS1. a Bioinformatic prediction of the potential binding site of miR-382–3p and STAT1. b Luciferase reporter assay analysis showing that the interaction with miR-382–3p and STAT1. c Spearman’s rank correlation showing the negative correlation between miR-382–3p and STAT1. d-e qPCR and western blot assay indicating that STAT1 was downregulated in the miR-382–3p overexpression PANC-1 and Mia paca2 cells. f-g CCK8 and clone formation eluted miR-382–3p overexpress could partly restrained the proliferation promoted by STAT1. h-i Cell scratch and transwell assay eluted miR-382–3p overexpress could partly restrained the migration and invasion promoted by STAT1