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. 2021 Jul 22;21:844. doi: 10.1186/s12885-021-08465-5

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© The Author(s) 2021

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. 3 — A MiR-411-3p is able to target HOXA10. miRmap and PicTar databases were applied to forecast the potential target genes. B The expression of possible mRNAs was examined upon PSMA3-AS1 knockdown and miR-411-3p overexpression. C The expression of three mRNAs was evaluated via RT-qPCR in glioma cell lines with the help of two-way ANOVA and Tukey analysis. D The binding sites of miR-411-3p and HOXA10 were presented by ENCORI database. E Luciferase reporter assay was performed to confirm the binding situation between miR-411-3p and HOXA10 using two-way ANOVA and Tukey analysis. F The connection among PSMA3-AS1, miR-411-3p and HOXA10 was testified by RIP assay. **P < 0.01