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. 2021 Jun 18;8:654766. doi: 10.3389/fmolb.2021.654766

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Copyright © 2021 Li, Luo, Huttad, Zhang, Wang, Feng, Ding and Han.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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RIPK4 inhibits EMT progression and STAT3 pathway activation in HCC. (A) Western blotting analysis of the expression levels of E-Cadherin, N-Cadherin, Vimentin, Zeb-1 protein in Huh7 and Hep3B cells infected with Lv-con and Lv-RIPK4 lentivirus, and ß-actin was used as a control. (B) Western blotting analysis of STAT3, p-STAT3, MMP-2, MMP-9 protein expression levels in Huh7 and Hep3B cells infected with Lv-con and Lv-RIPK4 lentivirus, and ß-actin was used as a control. (C) Representative images of huh7 morphology with Lv-con and Lv-RIPK4 lentivirus. (D,E) Representative images of lung metastases in mice and statistical analysis of the number of metastases. (F) Representative H&E staining pictures of mouse lung metastatic nodules. The data are expressed as mean ± SD. **p < 0.01; ***p < 0.001.