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. 2018 Jun 4;9(6):675. doi: 10.1038/s41419-018-0591-0

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© The Author(s) 2018

Open Access This 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 license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license 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 license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 4 — a Orthotopic transplantation tumor model analyzed the role of DDX39 on tumor growth and lung metastasis, representative images of tumors derived from Hep3B with DDX39 overexpression or knockdown in lung and liver. b HE staining of tumors derived from Hep3B with DDX39 overexpression or knockdown in lung. c Kaplan–Meier analysis of survival for mice transplanted with Hep3B with DDX39 overexpression or knockdown. d The activity of AST and ALT in blood of mice transplanted with Hep3B with DDX39 overexpression or knockdown. *p < 0.05