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. 2020 Oct 14;20:998. doi: 10.1186/s12885-020-07394-z

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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. 5 — MiR-142-3p suppression or USP6NL overexpression abolishes the effect of LINC00689 silence on TNBC cell proliferation and apoptosis. a. The expression of LINC00689 was measured by RT-qPCR in the context of LINC00689 knockdown. b. RT-qPCR determined the expression of USP6NL in TNBC cells transfected with pcDNA3.1 or pcDNA3.1/USP6NL. c. The colony formation assay detected the effect of inhibited miR-142-3p or upregulated USP6NL on LINC00689 silence-mediated cell proliferation. d-f. Flow cytometry analysis, JC-1 assay and TUNEL assay evaluated the apoptosis of cells under diverse conditions. The X axis of the FACS dot plots in Fig. 5d meant cells labelled with FITC and the Y axis indicated cells dyed by PI. **P < 0.01