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. 2020 May 11;11(5):345. doi: 10.1038/s41419-020-2501-5

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© The Author(s) 2020

Open Access This 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 license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license 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 license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 6 — a OC2 knockdown reduced the protein levels of the VEGFA/EGFL6 axis and the AKT/MAPK pathways in Caov3 and Skov3, followed by Western blotting assay. b CCK-8 assay showed that OC2 knockdown could inhibit Caov3 and Skov3 proliferation. c Representative images and quantitation of HUVECs tube formation. d Effect of OC2 knockdown on xenograft tumor growth from Skov3, the stripped tumors, tumor size and tumor weight as indicated (n = 4). e Representative images and quantitation of the microvessels and the OC2/VEGFA/EGFL6 axis in stripped tumors, followed by IHC assay. The tubes (c) and spots (e) were calculated by ImageJ software and statistically analyzed in five random fields; scale bars: 50 μm (c), 100 μm (e). Data are shown as mean ± SD of three independent experiments. *P < 0.05; **P < 0.01. (i) Caov3, (ii) Skov3.