NSC12 modulates the transcriptome signature in WM cells, resulting in antiproliferative and proapoptotic phenotype. (A) Heatmaps of differentially expressed protein-coding transcripts in BCWM.1 (325 upregulated, 1586 downregulated) and MWCL.1 cells (269 upregulated, 614 downregulated). Blue-red color scale was used to set rows with mean zero and SD one. Genes selected at q value 0 and fold change >2. Plot of the 20 most significant differentially expressed protein coding gene lists enriched in BCWM.1 and MWCL.1 (GO-BP terms). (B) Cytofluorimetric analysis of cell cycle performed using BCWM.1 and MWCL.1 exposed to NSC12 (0 to 6 μM; 12 hours). Average of triplicate experiments ± SD is shown. (C) Annexin V/PI staining was performed using BCWM.1 and MWCL.1 cells exposed to NSC12 (0 to 6 μM; 24 hours). Percent of both dead cells and viable cells is shown. Average of triplicate experiments ± SD is shown. (D) BCWM.1 and MWCL.1 cells were cultured in the presence or absence of NSC12 (0 to 6 μM; 24 hours). WM cells were then harvested, and cell lysates were subjected to western blot using anti-PARP, -Caspase 8, and -GAPDH antibodies. (E) BCWM.1 and MWCL.1 cells were exposed to NSC12 (6 μM) for 12 hours and subjected to wide transcriptome profiling, showing a significant inhibition of oxidative stress response-related gene sets, as shown by performing GSEA (P < .05; FDR < 25%). (F) BCWM.1 and MWCL.1 cells were treated with NSC12 (0 to 6 μM) for 12 hours and subjected to cytofluorimetric analysis of mtROS production (Mitosox). (G) BCWM.1 and MWCL.1 cells were cultured in the presence or absence of NSC12 (0 to 6 μM; 12 hours). WM cells were then harvested, and cell lysates were subjected to western blot using anti-H2AX, -NRF2, and -GAPDH antibodies.