Fig. 4: YAP is involved in HCC growth promoted by high viscoelasticity.
From: Matrix viscoelasticity promotes liver cancer progression in the pre-cirrhotic liver
a, Analyses of bulk RNA-seq data from mice fed a chow or FFD diet or a HiAD diet with vehicle treatment (n = 3 each), mice fed a HiAD with PM treatment (n = 2) and RAGEHepKO mice fed a HiAD (n = 3). The heat map shows enrichment in several YAP/TAZ target genes in the HiAD group compared with in the other groups. Tensin 1 (Tns1, red) target of interest. b, Schematic of the NASH-related HCC model combined with YAP inhibition. The diagram was created using BioRender. c, GS/MYC-tag immunohistochemistry on subsequent slides showing transformed foci (circles, top and middle). Active non-phosphorylated YAP (red) localized to the nuclei of GS positive cells (green) in control-vector-injected (for dn-TEAD2) mice fed a HiAD (bottom). Scale bars, 300 μm (top and middle) and 100 μm (bottom). NC, empty vector. d, Quantification of GS+MYC+ foci in c. n = 5. e, YAP targets Ctgf and Cyr61 were downregulated in dn-TEAD2-treated mice. n = 5. Data are mean ± s.e.m. n values refer to individual mice. Statistical analysis was performed using one-way ANOVA followed by Tukey’s multiple-comparison test.
