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. 2021 Jan 7;12:18. doi: 10.1186/s13287-020-02075-x

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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-26a-5p was a target and was negatively regulated by NORAD. a StarBase online provided the putative binding sites of NORAD and miR-26a-5p. b Dual-luciferase reporter gene assay was performed to confirm the binding between NORAD and miR-26a-5p. c The miR-26a-5p expression in bone marrow samples from patients with SONFH (n = 20) and femoral neck fracture (control, n = 20) was detected by RT-qPCR. d The correlation between NORAD expression and miR-26a-5p expression in patients with SONFH was analyzed by Spearman’s correlation analysis. e The miR-26a-5p expression in hBMSCs was detected by RT-qPCR. **P < 0.01 compared with control group, ^##P < 0.01 compared with Vector and si-NC group