Fig. 4: YAP signaling is a potent driver of the onset and progression of chondrosarcoma. | Cell Death & Disease

Fig. 4: YAP signaling is a potent driver of the onset and progression of chondrosarcoma.

From: Mice with Trp53 and Rb1 deficiency in chondrocytes spontaneously develop chondrosarcoma via overactivation of YAP signaling

Fig. 4

A Volcano plot of transcriptome profiles between human chondrosarcoma cell lines and controls from GSE48420. B KEGG analysis of the chondrosarcoma RNA-seq data showing the top 20 enriched pathways. Red box directs to Hippo pathway. C IHC analysis of the expression of YAP in human normal cartilage (control) and chondrosarcoma (hCHS) samples. Quantitative analysis was at right by Image J software. N = 12. D YAP expression in chondrosarcoma tissues (mCHS) from Col2-Cre;Trp53f/f/Rb1f/f mice compared to adjacent normal cartilage (control). E Schematic presentation of primary chondrosarcoma cells from Col2-Cre;Trp53f/f/Rb1f/f mice. F Representative images of immunofluorescent staining of YAP in primary chondrosarcoma cells. Scale bars, 50 μm. G The primary chondrosarcoma cells from Col2-Cre;Trp53f/f/Rb1f/f mice or primary chondrocytes from Col2-Cre mice were co-transfected with a luciferase reporter and pRL-TK plasmids (internal control) as indicated, respectively. After transfection of 48 h, the luciferase activities were identified by the Dual-Luciferase Assay Kit. H Soft agar analysis after silence of YAP using two different YAP lentivirus in primary chondrosarcoma cells from Col2-Cre;Trp53f/f/Rb1f/f mice as indicated. The corresponding quantification is identified on the right. N = 3. I–K The analyses of migration (I), invasion (J), and tumorsphere (K) after silence of YAP in primary chondrosarcoma cells as above. The corresponding quantification is identified on the right. N = 3. Error bars were the means ± SEM from three independent experiments. *P < 0.05, **P < 0.01.

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