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. 2021 Dec 19;21:684. doi: 10.1186/s12935-021-02379-9

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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 — Exosomal miR-663b promotes angiogenesis in-vivo. A Comparison of the tumors (CaSki) taken from the Exo-miR-663b up, Exo-up NC, Exo-miR-663b inh, Exo-inh NC groups. An equal volume of PBS was injected as a blank control. B Growth curves of tumors were generated by measuring tumor volumes every three days (n = 6). C Analysis of tumor weight in each group (n = 6). D IHC was performed to measure the expression level of VCL in tumors (CaSki) taken from the Exo-miR-663b up, Exo-up NC, Exo-miR-663b inh, Exo-inh NC groups. E IHC was performed to demonstrate the existence of endothelial tissue and to assess tumor angiogenesis using a CD31 antibody. *P < 0.05, **P < 0.01 and ***P < 0.001. VCL, vinculin