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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. 2 — PSMA3-AS1 functions as a ceRNA for miR-411-3p. A-B Subcellular fractionation and FISH assays were used to confirm the location of PSMA3-AS1 in glioma cells. C The possible target genes of PSMA3-AS1 were predicted via ENCORI database. D RNA pull down assay was carried out to confirm the interaction between PSMA3-AS1 and potential miRNAs. E The binding sites were displayed with the help of ENCORI database. F RIP assay was used to test the correlation between PSMA3-AS1 and miR-411-3p. G RT-qPCR was implemented to assess the overexpression efficiency of miR-411-3p. H Luciferase reporter assay was conducted to test the interaction between PSMA3-AS1 and miR-411-3p using two-way ANOVA and Tukey methods. **P < 0.01