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. 2021 Jan 25;40:41. doi: 10.1186/s13046-021-01844-7

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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. 2 — CBR3-AS1 affects breast cancer cell drug resistance. a, b P-gp expression was measured by western blot after CBR3-AS1 was overexpressed or silenced. The drug treatments comprised 100 nM ADR to MCF-7 cells and 30 μM ADR to MCF-7/ADR cells before culture for 48 h. c, d The fluorescence intensity of ADR was detected by flow cytometry, showing intracellular ADR accumulation. e, f Drug resistance was examined by CCK-8 assays in cells transfected with CBR3-AS1 overexpression plasmid or siRNAs. g, h Cells transfected with the CBR3-AS1 overexpression plasmid or siRNAs were seeded onto plates. The number of colonies was counted on the 14th day after seeding. i Apoptosis rates of MCF-7 cells treated with 100 nM ADR were detected. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001