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. 2020 Sep 14;20:878. doi: 10.1186/s12885-020-07343-w

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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. 3 — ANGPTL4 overexpression decreases the mRNA levels of ECM-related genes. a Next-generation RNA sequencing revealed that genes related to adherens junctions, blood vessel morphogenesis, extracellular matrix and wound healing were most affected by ANGPTL4 overexpression. b Real-time quantitative PCR confirmed that ten genes were downregulated in the 231 ANGPTL4 OE group compared with the control group. These results suggest that ANGPTL4 overexpression might affect TNBC progression by inhibiting ECM-related genes (Graghpad Prism statistical software package, version 5.01, *p < 0.05)