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. 2018 Jun 1;18:621. doi: 10.1186/s12885-018-4326-5

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© The Author(s). 2018

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided 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 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.

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Fig. 4 — Slit3 negatively regulated HCC cell growth in vivo. a Stable Slit3 repressed clones (LM3-shSlit3) displayed induced tumor growth when compared with the control cells (LM-shCTL) 6 weeks post-injection of cells subcutaneously into flank region of nude mice (n = 5). b Stable Slit3 overexpressed clones (Hep3B-Slit3) displayed impaired tumor growth when compared with the control cells (Hep3B-pcDNA) 6 weeks post-injection of cells subcutaneously into flank region of nude mice (n = 5). c Immunohistochemical staining of Slit3, CD31, p27, β-catenin and phosopho-GSK3β (ser9) in tumor formed by LM3-shCTL and LM3-shSlit3 stable cells. d Immunohistochemical staining of Slit3, CD31, p27, β-catenin and phosopho-GSK3β (ser9) in tumor formed by Hep3B-pcDNA and Hep3B-Slit3 stable cells. Representative results from two mice of each group were shown