Figure 3.
NSC12 mediates inhibition of MYD88 in WM cells. (A) 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 PI3K-AKT-mTOR- and MYD88-related gene sets, as shown by performing GSEA (P < .05; FDR < 25%). (B) BCWM.1 and MWCL.1 cells were cultured in the presence or absence of NSC12 (0 to 6 μM; 6 hours). WM cells were then harvested, and cell lysates were subjected to western blot using anti-MYD88, -p-SYK, -SYK, -p-BTK, -BTK, and -GAPDH antibodies. (C) BCWM.1 and MWCL.1 cells were treated with NSC12 (0 to 6 μM; 6 hours), subjected to RNA extraction, and evaluated for MYD88 and HCK mRNA levels by using qRT-PCR (2−ΔΔCt), with normalization to GAPDH (P, P values). (D) BCWM.1 and MWCL.1 cells were cultured in the presence or absence of NSC12 (0 to 6 μM; 6 hours). WM cells were then harvested, and cell lysates were subjected to western blot using anti-c-Myc and -GAPDH antibodies.

NSC12 mediates inhibition of MYD88 in WM cells. (A) 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 PI3K-AKT-mTOR- and MYD88-related gene sets, as shown by performing GSEA (P < .05; FDR < 25%). (B) BCWM.1 and MWCL.1 cells were cultured in the presence or absence of NSC12 (0 to 6 μM; 6 hours). WM cells were then harvested, and cell lysates were subjected to western blot using anti-MYD88, -p-SYK, -SYK, -p-BTK, -BTK, and -GAPDH antibodies. (C) BCWM.1 and MWCL.1 cells were treated with NSC12 (0 to 6 μM; 6 hours), subjected to RNA extraction, and evaluated for MYD88 and HCK mRNA levels by using qRT-PCR (2−ΔΔCt), with normalization to GAPDH (P, P values). (D) BCWM.1 and MWCL.1 cells were cultured in the presence or absence of NSC12 (0 to 6 μM; 6 hours). WM cells were then harvested, and cell lysates were subjected to western blot using anti-c-Myc and -GAPDH antibodies.

Close Modal

or Create an Account

Close Modal
Close Modal