Fig. 2: M-100 specifically induces apoptosis in murine lymphoma B-cells but not activated wild-type B-cells.
From: Targeting the MYC interaction network in B-cell lymphoma via histone deacetylase 6 inhibition
A Apoptosis detection using Annexin V and PI staining. Eµ-Myc lymphoma and activated (10 µg LPS/ml) wild-type mouse B-cells were compared. B Representative cell cycle analysis of Eµ-Myc lymphoma and activated B-cells treated for 72 h. C Cell cycle analysis from B was quantified. Two-Way ANOVA (Sidak’s posthoc). D Gene expression changes of Eµ-Myc lymphoma or activated wild-type (WT) B-cells cells treated for 24 h with 4 µM M-100 using quantitative real-time PCR analysis. One-Way ANOVA (Tukey’s posthoc). E Western Blot analysis of activated wild-type B-cells or Eµ-Myc lymphoma cells treated with M-100 for 24 h. Gapdh and actin were used as loading controls. Ac-tub - acetylated tubulin. F Apoptosis was analyzed in activated wild-type B-cells treated with 4 µM M-100, 0.5 µM BCL-2 inhibitor (BCL-2i) Venetoclax or both for 24 h. One-Way ANOVA (Tukey’s posthoc). G CH12F3 cells were analyzed regarding viability (Annexin V/PI staining) and cell cycle after treatment with 2 µM M-100 for 48 h. Activation was performed using 1 µg/ml CD40L, 5 ng/ml IL-4, and 1 ng/ml TGF-β and added 2 h after M-100 treatment. CH12F3 cells harbor no MYC translocation. Two-Way ANOVA (Sidak’s posthoc). Data in A–G are representative of at least n = 3 independent experiments. Data represent mean + SEM, if applicable. *P < 0.05, ***P < 0.001, ns - not significant.
