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. 2022 Jun 5;13(5):13571–13586. doi: 10.1080/21655979.2022.2080385

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© 2022 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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Figure 7. — Verification of the chemoresistance mechanism of PCK1 and the benefit of combination therapy in vivo.

A. Nude mice model of subcutaneous tumorigenesis. B. Size of subcutaneous tumor tissues. C. Volume of tumor tissues: the combination group is the lowest. D. Weight of tumor tissues: the combination group is the lowest. E. Immunohistochemical results: the immunohistochemical staining of KEAP1 and PCK1 is shown in yellow; blue represents the nuclei (DAPI). In non-drug resistant tissues (P), the expression of PCK1 increased and that of KEAP1 decreased after using vemurafenib. In resistant tissues (R), the level of PCK1 was higher than that in P; the combination of 3-MPA+vemurafenib decreased the levels of PCK1 and increased the levels of KEAP1.