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. 2021 May 27;19:224. doi: 10.1186/s12967-021-02881-8

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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. 4 — miR-449a interacts with KDM3A; HIF-1α could bind with KDM3A. a RT-qPCR and Western blot analyzed KDM3A expression in cells after overexpression of miR-449a; b Bioinformatics website predicted the binding sites of miR-449a and KDM3A; c Luciferase reporter gene experiment verified the relation between miR-449a and KDM3A; d RT-qPCR and Western blot analyzed HIF-1α expression in cells after overexpression of KDM3A; e. CO-IP assay analyzed the interaction between KDM3A and HIF-1α; The data from three independent experiments were expressed as mean ± standard deviation. *P < 0.05 compared with the the NC-mimic group; #P < 0.05 compared with the the oe-NC group