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. 2019 Dec 5;19:1192. doi: 10.1186/s12885-019-6362-1

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© The Author(s). 2019

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 — Migration and proliferation ability of HSC is related to CCN3-ERK signaling. There was no significant difference in OS and CRR between patients with or without cirrhosis (a). Recombinant CCN3 could significantly enhance the migration and proliferation (c) of LX2, which could be reversed by S (sorafenib) or U (U0126) (b). The diminished number of HSC and subcutaneous tumor weight were found in mice injected with MHCC97H-CCN3-sh cells in nude mouse models (d). The increased number of HSC and the enhanced subcutaneous tumor growth were found in the MHCC97H-CCN3 group (e). CCN3 could activate ERK signaling pathways with upregulation of RAF, p-RAF, p-MEK and p-ERK, and sorafenib or U0126 showed significant inhibition on ERK signaling (f)