Skip to main content
. 2017 Jan 5;12(1):e0169407. doi: 10.1371/journal.pone.0169407

Fig 2. Quisinostat-mediated HDAC inhibition results in a dissociation of the driving complex in synovial sarcoma.

Fig 2

(A, B) Proximity ligation assay of SS18-SSX/TLE1 nuclear signal demonstrates a significant decrease in detectable protein co-localization following HDAC inhibition in SYO-1 synovial sarcoma cells. (C) Quisinostat treatment at 0.025 μM reactivates targets of SS18-SSX-mediated gene repression, EGR1 and CDKN2A, in six human synovial sarcoma cell lines. (D) Expression of EGR1, p16INKa and p14ARF (CDKN2A) protein levels increase with increasing concentrations of quisinostat, concomitant with a decrease in SS18-SSX protein levels. GAPDH was used as a loading control. Scale bars in panel A represent 20 μm. Statistical significance compared to vehicle treatment controls was determined by Student t test: * denotes p < 0.05. Error bars represent standard error of mean from conditions performed in triplicate.