Fig. 6
From: Molecular features and vulnerabilities of recurrent chordomas
HXR9-induced apoptosis is mediated via cFOS. Activation of cleaved Caspase-3/7 (488 nm; green channel) in U-CH11 (a) and U-CH11R (b) treated for 24 h with 30 μM CXR9 or HXR9. The percentage of cleaved Caspase 3/7 positive cells following each treatment was determined by cell counts of representative image sections (n = 12; c). Immunoblots showing cleaved PARP, Procaspase 3, cleaved Caspase-3 and cleaved Caspase-7 in chordoma cell lines treated with 30 μM of HXR9 or CXR9 for 24 h (d). CFOS expression levels in response to treatment with HXR9 or two control compounds (CXR9 and DMSO) in U-CH1 versus U-CH19 (e) and U-CH11 compared to U-CH11R (f) cell lines quantified by qRT-PCR and normalized against GAPDH. Gene expression experiments were performed in technical and biological triplicates. Statistical differences were determined by Student’s t-tests (*p < 0.05, **p < 0.01, ***p < 0.001)