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. 2020 Jun 3;20:210. doi: 10.1186/s12935-020-01298-5

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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. 11 — Effects of HSD17B6 overexpression on the cell proliferation, migration and invasion of HepG2 cells. a HSD17B6 expression in HepG2 was upregulated through lentivirus transfection. b CCK8 assay were performed to analyze the effect of HSD17B6 overexpression on HepG2 cell growth in vitro. Data are expressed as mean ± SD of 3 experiments (*p < 0.05). c, d Wound–healing assay was performed to analyze the effect of HSD17B6 overexpression on HepG2 cell migration (*p < 0.05). e, f Transwell assay was performed to analyze the effect of HSD17B6 overexpression on HepG2 cell invasion in vitro (**p < 0.01)