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. 2021 Nov 8;40:352. doi: 10.1186/s13046-021-02110-6

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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. 8 — In vivo role of DNMT1/miR-378a-3p/TRAF1/p65 in regulating HCC angiogenesis. A-C Tumor growth of mice subcutaneously implanted with treated HCCLM3 cells. Tumor volume and weight were measured, and tumor size is shown. D Immunohistochemical staining of CD34, DNMT1, TRAF1, p65 and VEGF in the tumors from subcutaneously implanted mice. E FISH assay for miR-378a-3p and immunohistochemical staining for DNMT1, TRAF1, p65, VEGF and CD34 were performed on 10 human HCC specimens. F A working model showing how miR-378a-3p inhibits HCC tumor angiogenesis by inactivating the NF-κB signaling pathway. *P < 0.05; **P < 0.01; ***P < 0.001