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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. 3 — HK-2 is identified as a downstream target of SALL4. a Verification of microarray results for differentially expressed genes between control and SALL4 knockdown MGC-803 cells. b, c Luciferase reporter assays for the relative luciferase activity of HK-2 gene promoter. d ChIP assay for the binding of SALL4 to the promoter region of HK-2 gene. e The changes in levels of hexokinase activity in control and SALL4 knockdown and overexpressing gastric cancer cells. Vertical bars represented SD of the mean values (n = 3); *P < 0.05, **P < 0.01, ***P < 0.001