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. 2020 May 24;20:188. doi: 10.1186/s12935-020-01275-y

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© The Author(s) 2020

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 — HK-2 mediates the promoting role of SALL4 in gastric cancer cells proliferation, migration and invasion. a, d Cell colony formation assay for the growth ability of SALL4-overexpressing HGC-27 and AGS cells with or without HK-2 knockdown. b, e Cell counting assay for the growth ability of SALL4-overexpressing HGC-27 and AGS cells with or without HK-2 knockdown. c, f Transwell migration and matrigel invasion assays for the migration and invasion abilities of SALL4-overexpressing HGC-27 and AGS cells with or without HK-2 knockdown. Vertical bars represented SD of the mean values (n = 3); *P < 0.05, **P < 0.01, ***P < 0.001