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. 2017 Apr 13;16:78. doi: 10.1186/s12943-017-0639-2

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© The Author(s). 2017

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. 3 — The function of DC-SIGNR in vitro. a, cell proliferation was measured by MTT assay. BGC823 cells were infected with sh-DC-SIGNR. SGC7901 cells were infected with DC-SIGNR mediated by lentivirus. b colony-forming growth assays were performed to determine the proliferation of sh-DC-SIGNR infected BGC823 cells and DC-SIGNR mediated by lentivirus infected SGC7901 cells. Colonies were counted and captured. c wound-healing assays were conducted to determine the rate of migration by measuring the distance from one edge of the wound to the other side. d transwell assays were conducted to investigate changes in BGC823 cells and SGC7901 cells migration and invasion. All experiments were performed in biologic triplicates with three technical replicates; *P < 0.05, **P < 0.01 and ***P < 0.001