Fig. 2: The EZH2 inhibitor SHR2554 mediates therapeutic effects in TCL by reducing H3K27me3 levels.
A Dose-response curves for SHR were generated across 5 TCL cell lines. SHR was diluted from an initial concentration of 50 μM and treated at a density of 4 × 103 cells/mL/well for 144 h. The control group received the same concentration of DMSO. The 144-hour 50% inhibitory concentration (IC50) values were calculated using SPSS and are presented accordingly. B Western blot analysis was performed to assess the levels of H3K27me3 and H3K27ac following treatment with SHR for 72 h. H3 was used as a loading control. C, D 1 × 105 cells/mL were cultured in the presence of the indicated concentrations of SHR for 72 h. Cell apoptosis (C) and cell cycle (D) were assessed by flow cytometry. E, F Western blot analysis was performed to assess cell apoptosis (E) and cell cycle-related proteins (F). GAPDH was used as a loading control. G Volcano plot illustrating the changes in gene expression in the SHR group (SHR 5 μM, 72 h) compared to the control group in RNA-seq. H KEGG enrichment of regulated genes in the SHR group compared to the control group. I, J Gene set enrichment (GSEA) plot of BENPORATH_ES_WITH_H3K27ME3 (I) and SENESE_HDAC1_AND_HDAC2_TARGETS_DN (J) gene sets comparing SHR and the control group. SHR, SHR2554. All experiments were conducted in triplicate., and data are reported as mean ± SD. Experimental groups were compared to the DMSO control using One-Way ANOVA followed by LSD post hoc multiple comparisons. *p < 0.05, **p < 0.01, ***p < 0.001, compared with the control group.
