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. 2021 Jan 6;21:14. doi: 10.1186/s12935-020-01698-7

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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. 4 — ShPCAT6 inhibited tumor growth and BRD4 expression, and promoted apoptosis and miR-139-3p expression in tumor tissues. a–c The picture of the solid tumor (a) was exhibited; tumor volume (b) and tumor weight (c) were calculated. d Cell apoptosis in tumor tissues was detected by TUNEL staining (Magnification × 400). e The expression of BRD4 in tumor tissues was detected by immunohistochemical (Magnification × 400). f The expression of miR-139-3p was detected by RT-qPCR. g The protein levels of EMT-related proteins were detected by Western blot. U6 was used as an internal control. (^***P < 0.001, vs. shNC). shNC shRNA negative control