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. 2020 May 28;9(5):54. doi: 10.1038/s41389-020-0242-z

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© The Author(s) 2020

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. 3 — a The metastatic potential of HCCLM3 orthotopic nude mice model with different lncRNA-SOX2OT level was evaluated by PET scan. SOX2OT overexpression enhanced intrahepatic, mesenteric and pulmonary metastasis. Conversely, the depletion of SOX2OT clocked metastasis. b Ectopic expression of lncRNA-SOX2OT significantly induced the number of CTCs (GFP labeled). The depletion of lncRNA-SOX2OT reduced the number of CTCs. c Overexpression of lncRNA-SOX2OT resulted in greater liver metastases burden, while the depletion of lncRNA-SOX2OT decreased the liver metastases burden in HCCLM3 cells. d, e lncRNA-SOX2OT overexpression increased the lung metastases burden, while the depletion of lncRNA-SOX2OT significantly reduced the lung metastases burden of HCCLM3 cells.