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. 2022 Feb 8;22:65. doi: 10.1186/s12935-022-02479-0

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© The Author(s) 2022

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. 3 — PTPN14 suppresses HCC invasion and migration in vitro and in vivo. The migration and invasion of HepG2 cells with stable PTPN14 knockdown (A) and SK-Hep1 cells with PTPN14 stable overexpression (B) was assessed by a Transwell assay. The number of migrating and invading cells was counted in at least three different fields per sample. The data are shown as the means ± SD (n = 3). *p < 0.05; **p < 0.01 compared with the respective controls. C The pulmonary metastasis of HepG2 cells with stable PTPN14 knockdown and SK-Hep1 cells with PTPN14 stable overexpression was monitored by bioluminescence imaging in vivo. Pulmonary metastasis was observed using a whole-body fluorescent imaging system. Right, gross view of lung metastatic nodules. Relative photon flux of the two groups was calculated. The data are shown as the mean ± SD (n = 5). **p < 0.01 compared with the respective controls