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. 2019 Dec 6;4:54. doi: 10.1038/s41392-019-0082-5

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© The Author(s) 2019

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 — Forced expression of DKK1 promotes tumor formation by HepG2 and HUH-7 cells in vivo. Compared with control conditions, downregulation of DKK1 in HepG2 and HUH-7 cells significantly diminished in vivo tumor formation. Control HepG2 and HUH-7 cells transfected with scrambled shRNA generated large tumors on the right flanks of nude mice (green arrow), while smaller tumors were observed on the left flanks of mice injected with DKK1-shRNA-transfected HepG2 and HUH-7 cells (red arrow) (a, left panel). The volumes of tumors in the recipient mice are shown (a, right panel). Forced expression of DKK1 in HCC cells produced significantly enhanced in vivo growth of tumors on the left flanks of the nude mice (red arrow) compared with tumors on the right flanks of mice injected with control cells (green arrow) (b, left panel); the volumes of tumors in the recipient mice are shown (b, right panel). *P < 0.05