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. 2022 Jun 27;17:332. doi: 10.1186/s13018-022-03181-7

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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. 5 — EBF1 activates FGA5-AS1 expression in osteosarcoma cells. A DNA pull-down assay detected the binding situation of EBF1 and FGA5-AS1 promoter. B EBF1 expression was inhibited in osteosarcoma cells. C FGA5-AS1 expression was tested via RT-qPCR when EBF1 was silenced. D The binding sites of FGA5-AS1 promoter and EBF1. E Luciferase reporter assay was performed to verify the binding sites of FGA5-AS1 promoter and EBF1. F The proliferation of osteosarcoma cells was assessed by immunofluorescence assay after EBF1 was prohibited. G Cell apoptosis upon EBF1 silencing was assessed by caspase-3/8/9 assay. H Cell invasion after EBF1 knockdown was verified by transwell assay. ^**P < 0.01