Supplementary Figure 7: Tumor and cell line effects of TNFR2 p.Thr377Ile and pathway inhibition.
From: Genomic analysis of mycosis fungoides and Sézary syndrome identifies recurrent alterations in TNFR2
(a) Graph of the tumor volumes of subcutaneous tumors generated with Jurkat cells expressing empty vector (EV), wild-type TNFR2 (WT) or mutant TNFR2 (MT). The TNFR2 MT tumor volumes are significantly larger over time compared to the EV controls (P = 0.002), as are the TNFR2 WT volumes (P = 0.04); n = 10 mice per group, total of 30 mice, mean ± standard error shown. Asterisks are used to indicate the results of ANOVA analysis: *P < 0.05, **P < 0.01, ***P < 0.0001, ****P < 0.00001. (b) Dose-response curves of Jurkat cells expressing EV, TNFR2 WT or TNFR2 MT upon treatment with bortezomib for 24 h; n = 3 biological replicates. Mean ± standard error shown. (c) Control or TNFR2-knockout (KO) HH cells stained with TNFR2 antibody or isotype control and analyzed by flow cytometry. (d) Dose-response curves of control or TNFR2 KO HH cells upon treatment with bortezomib for 24 h; n = 3 biological replicates. Mean ± standard error shown. (e) Cell viability of CRISPR control and TNFR2 KO cells over 4 d. There was no significant difference observed. (f) Dose-response curves of the HH CTCL cell line and the Hut78 CTCL cell line exposed to bortezomib treatment for 24 h; n = 3 biological replicates. Mean ± standard error shown.
