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. 2022 Jun 3;41:192. doi: 10.1186/s13046-022-02394-2

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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. 11 — Summary of the oncogenic potential of TAZ in the mouse liver depending on its crosstalk with other genes. (A) Combined overexpression of myristoylated/activated AKT (AKT) and TAZS89A (a variant that escapes phosphorylation-mediated degradation by LATS1/2 proteins) drives the transdifferentiation of hepatocytes into malignant cholangiocytes, leading to intrahepatic cholangiocarcinoma development by 8-10 weeks post-injection. (B) Simultaneous overexpression of AKT and TAZS89AS51A (TAZS51A; a mutant form of TAZ that cannot bind to TEAD transcription factors) leads to the induction of clusters of lipid-rich and enlarged hepatocytes that are indistinguishable from those generated by transfection of AKT alone. (C) Overexpression of AKT and TAZS89A together with a dominant-negative form of the transcriptional regulator RBP-J (dnRBP-J) suppresses the NOTCH pathway, but does not impair AKT/TAZ-dependent liver carcinogenesis. Consequently, pure hepatocellular carcinoma lesions develop in AKT/TAZ/dnRBP-J mice by 13 weeks post-injection. (D) Suppression of YAP, the TAZ paralog, via short hairpin RNA delays cholangiocarcinogenesis in AKT/TAZ mice without affecting the tumor phenotype. Pure cholangiocarcinoma lesions form in AKT-shYAP-TAZ mice by 30 weeks post-injection. Abbreviations: w.p.i., weeks post-injection