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. 2022 Sep 15;20:138. doi: 10.1186/s12958-022-00998-z

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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 — MiR-28-5p deficiency recovered breast cell malignant behaviors suppressed by circ-CSNK1G1 silence. Rescue experiments were performed in MDA-MB-231 and BT-549 cells transfected with si-circ-CSNK1G1 alone or si-circ-CSNK1G1 + anti-miR-28-5p together, using si-NC or si-circ-CSNK1G1 + anti-miR-NC as the control. A The expression of miR-28-5p was detected using qPCR. B-D Cell proliferation was analyzed using MTT assay and colony formation assay. E Cell apoptosis was assessed using flow cytometry assay. F and G Cell migration and cell invasion were investigated using transwell assay. H-J Glucose consumption, lactate production and ATP/ADP ratios were detected to assess glycolysis progression. **P < 0.01, ***P < 0.001, and ****P < 0.0001