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. 2020 Sep 12;20:450. doi: 10.1186/s12935-020-01539-7

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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.1 — HKDC1 was upregulated in LUAD tissues and cells. a, b Oncomine (a) and UALCAN (b) data showed that HKDC1 was highly expressed in LUAD tissues compared with normal tissues. c The HKDC1 mRNA expression level was significantly elevated in LUAD tissues compared with normal lung tissues in 20 paired fresh tissues. d, e The HKDC1 expression level was obviously higher in the LUAD cell lines than in the normal human lung epithelial cell line HBE on mRNA (d) and protein level (e). Data were expressed as the mean ± standard deviation (mean ± SD) **p < 0.01