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. 2020 Aug 18;20:400. doi: 10.1186/s12935-020-01492-5

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© The Author(s) 2020

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. 8 — The repression of miR-578 up-regulation on BC progression in vitro was mediated by HIF1A. a HIF1A protein level by western blot in MCF7 and BT-549 cell lines transfected with vector or HIF1A. MCF7 and BT-549 cell lines were transfected with miR-NC mimic + vector, miR-578 mimic + vector or miR-578 mimic + HIF1A, followed by the determination of cell viability by CCK-8 assay (b), cell apoptosis by flow cytometry (c), cell migration and invasion by transwell assay (d, e), glucose uptake, lactate product and ATP level using assay kits (f–h). vector: negative control plasmid, HIF1A: recombinant HIF1A overexpressing plasmid. *P < 0.05