Fig. 3: Different human B-cell lymphoma cell lines respond to HDAC6 inhibition by initiating apoptosis and cell cycle arrest.
From: Targeting the MYC interaction network in B-cell lymphoma via histone deacetylase 6 inhibition

A Cell viability of human B-cell lymphoma cells after treatment with increasing concentrations of M-100 for 48 h using MTT assay. Non-linear regression (inhibitor vs. normalized response) was inserted. B Amount of Annexin V+ cells after treatment with 4 µM M-100 for 48 h. Unpaired Welch’s t-test, two-tailed. C Cell cycle analysis of cells treated with 4 µM M-100 for 48 h. Two-Way ANOVA (Sidak’s posthoc). D Different concentrations of M-100 were tested for inducing ac-H3 signals by Western blot. Vinculin was used as a loading control. E Ramos HDAC6 (HD6) knock-out (KO) cells were generated and compared to HDAC6 wild-type (WT) cells. Western Blot analysis shows absence of HDAC6. Actin serves as a loading control. F Proliferation was measured of Ramos HDAC6 WT and HDAC6 KO cells by cell counting, and normalized to WT cells at t = 72 h. Two-Way ANOVA (Sidak’s posthoc). G Dose-response curves were determined for Ramos HDAC6 WT and KO cells treated for 48 h with increasing concentrations of M-100 or ACY-1215 by MTT assay. Non-linear regression (inhibitor vs. normalized response) was inserted. Data in A–G are representative of at least n = 3 independent experiments. Data represent mean + SEM, if applicable. *P < 0.05, **P < 0.01, ***P < 0.001, ns not significant.