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. 2021 Jan 25;40:41. doi: 10.1186/s13046-021-01844-7

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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. 5 — Overexpression of CBR3-AS1 promotes ADR resistance in vivo. a In vivo experimental design. b CBR3-AS1 expression in the transplanted tumors. c miR-25-3p expression in the transplanted tumors. d Live imaging experiments showing transplanted tumor cells. e Representative images of tumors at 5 weeks after subcutaneous transplantation when mice were euthanized. f Tumor growth curves of the respective groups. g Tumor mass of the respective groups. h JNK1 and MEK4 protein expression was measured in the respective groups by western blot. I IHC analysis of the expression levels of JNK1 and MEK4 in the respective groups. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001