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. 2023 Jan 7;11:3. doi: 10.1186/s40364-022-00442-9

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© The Author(s) 2023

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 — CircEMB affects the malignant behaviors of OSA by sponging miR-3184-5p. a-c CCK-8 and colony formation assays showed that miR-3184-5p knockdown partly reversed circEMB knockdown-induced decrease in cell proliferation. d-e Transwell and wound healing assays revealed the mechanisms through which miR-3184-5p knockdown partly reversed circEMB-mediated invasion and migration abilities of 143B and U2OS cells. Scale bar, 100 μm Scale (Transwell); Scale bar, 200 μm(wound-healing assays). f Flow cytometry revealed that silencing miR-3184-5p partly reversed circEMB-mediated apoptosis of 143B and U2OS cells. g Flow cytometry revealed that silencing miR-3184-5p partly reversed circEMB-mediated G1/S phase arrest of 143B and U2OS cells. Data are expressed as mean ± SD (n = 3) (*, p < 0.05; **, p < 0.01; ***, p < 0.001)