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. 2021 Jan 12;19:22. doi: 10.1186/s12951-020-00767-3

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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. 5 — Overexpression of miR128-1, miR128-2 and miR421 promotes genomic instability, induces an S-phase arrest and promotes the growth of breast cancer cells. QRT-PCR detection of miR128-1, miR128-2 and miR421 expression in seven breast cancer cells and normal human mammary epithelial cells 184A1 and MCF-10A (a). QRT-PCR detection of miR128-1, miR128-2 and miR421 expression transfected with miRNAs mimics in MDA-MB-231 cells (b). The percentage of multinuclei and micronuclei in MDA-MB-231 cells after overexpression of miR128-1, miR128-2 and miR421 (c). Cell cycle distribution of MDA-MB-231 cells after overexpression of miR128-1, miR128-2 and miR421 (d). Cell growth curve of MDA-MB-231 cells with miR128-1, miR128-2 and miR421 overexpression (e)