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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. 4 — Silencing HKDC1 inhibited proliferation, invasion, and migration in vitro and tumorigenesis in vivo. a, b The mRNA (a) and protein level (b) of HKDC1 was detected after transfected with sh-HKDC1 in both A549 and H1299 cells. c The viability of LUAD cells with sh-HKDC1 was decreased by CCK-8 assay. d, e Knockdown of HKDC1 inhibited A549 (d) and H1299 (e) cells migration and invasion in vitro as assessed by the wound healing assay (scale bar, 100 μm). f HKDC1 knockdown inhibited tumor growth in vivo. Data were expressed as the mean ± standard deviation (mean ± SD) *p < 0.05, **p < 0.01