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. 2019 Oct 4;12:8217–8227. doi: 10.2147/OTT.S217468

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© 2019 Cheng et al.

This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License (http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms (https://www.dovepress.com/terms.php).

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CSC marker expression was affected by sorafenib therapy in the xenograft mouse model. Western blotting (left panel) and associated statistical analysis (right panel) for the expression of E-cadherin (E-cad), SALL4, and CD90 with or without sorafenib therapy in Chang liver (A), PLC/PRF/5 (B), and HepG2 (C) xenograft tumors revealed no significant change in CSC marker expression. Western blotting (left panel) and statistical analysis (right panel) for the expression of cytokeratin 7 (CK7) and cytokeratin 19 (CK19) with or without sorafenib therapy in Chang liver (D), PLC/PRF/5 (E) and HepG2 (F) xenograft tumors also revealed no significant change, except for significantly increased CK19 expression in HepG2 xenograft tumors.

Abbreviations: C, control group; S, sorafenib treated group.