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. 2022 Aug 10;22:876. doi: 10.1186/s12885-022-09970-x

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© The Author(s) 2022

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. 4 — The miR-26a-5p directly regulated the expression of HSDL2 in the Hela and C33A cells. (A) Sequence of HSDL2 3’-UTR binding to the miR-26a-5p was predicted by TargetScan and miRDB database. (B) The free energy score for binding between miR-26a-5p and HSDL2 mRNA was calculated using RNAhybird database. (C) Luciferase activity was analyzed in the Hela cells transfected miR-NC or miR-26a-5p mimic and HSDL2 3’-UTR wild type or mutant. The expression of HSDL2 mRNA and HSDL2 protein were analyzed in the Hela (D and E) and C33A cells (F and G) transfected miR-NC or miR-26a-5p mimic. All data were from three independence experiments (*p < 0.05, t-test)