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. 2021 Aug 21;7:218. doi: 10.1038/s41420-021-00604-y

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© The Author(s) 2021

Open Access This 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 license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license 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 license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 4 — A The nuclear and cytoplasmic fractions of circPDCD11 were assessed using RT-qPCR in TNBC cells (MDA-MB-468, BT549). B The downstream target element of circPDCD11 was predicted using CircInteractome (https://circinteractome.nia.nih.gov/), which revealed that miR-432-5p displayed the complementary binding sites for circPDCD11. C A luciferase reporter assay demonstrated the intermolecular interaction (firefly/Renilla) in 293 T cells transfected with circPDCD11 wild type or mutant and miR-432-5p mimics or controls. D RT-PCR demonstrated the expression of miR-432-5p in MDA-MB-468 cells transfected with a circPDCD11 knockdown (sh-circPDCD11) and in BT549 cells overexpressing circPDCD11 (circPDCD11 up). E Clinical correlation analysis calculated by Pearson’s correlation reflected the correlation between circPDCD11 and miR-432-5p in clinical samples (32 samples). The data are presented as the means ± SD. Asterisks indicate significant differences (**p < 0.01).