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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. 4 — HK-2 mediates the promotion of glycolysis by SALL4 in gastric cancer cells. a, b qRT-PCR and western blot analyzed the expression of SALL4, HK-2 and glycolytic related genes and proteins in SALL4-overexpressing HGC-27 cells and AGS cells with or without HK-2 knockdown. c, d The levels of glucose uptake, lactate production, lactate dehydrogenase activity, ATP level, and hexokinase activity in SALL4-overexpressing HGC-27 cells 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