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. 2020 Apr 26;20:137. doi: 10.1186/s12935-020-01221-y

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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 — KPNA2 is a target of miR-144-3p. a qRT-PCR and b, c Western blot were conducted to determine miR-144-3p and KPNA2 levels in breast cancer cell lines MCF-7 and MDA-MB-157 and human normal breast epithelial cell line MCF 10A, respectively. d RIP and e dual-luciferase reporter assay were carried out for validation of the combination between miR-144-3p and KPNA2, and f their potential targeted binding sites were predicted by a bioinformatics database. Mimic NC and miR-144-3p mimic were transfected into cells, and the levels of g miR-144-3p and h, i KPNA2 were test again in cells (*p < 0.05)