Extended Data Fig. 6: PBRM1-deficient tumors depend on SMARCA4 and ARID2 for NF-κB activity and tumor formation.
a) NCC432 cells expressing either empty vector (EV) or PBRM1 were treated with SMARCA2/4 ATPase inhibitor BRM014 for 3 days and the expression of NF-κB targets was evaluated by RT-qPCR (n = 3 technical replicates representative of 2 biological replicates). Data are presented as mean values + /- s.d. b) Colony formation of 786-O cells expressing shRNA against non-targeting control (NTC) or ARID2. c) Colony formation of 786-O cells expressing shRNA against non-targeting control (NTC) or SMARCA4. d) Immunoblotting and e) colony formation of NCC432 cells expressing shRNA against non-targeting control (NTC) or ARID2 (n = 3 biological replicates). Data are presented as mean values + /- s.d. P-value (two-sided test). f) Immunoblotting and g) colony formation of NCC432 cells expressing shRNA against non-targeting control (NTC) or SMARCA4 (n = 4 biological replicates). Data are presented as mean values + /- s.d. *p < 0.05, **p < 0.01, ***p < 0.001, **** p < 0.0001 (two-sided t-test). In vivo tumor formation in h) 786-O parental cells and i) 786-O PBRM1 KO cells expressing shRNA against Non-targeting control (NTC), ARID2 (clone 1) or SMARCA4 (clone 2) (n = 10 tumors per group). Data are presented as mean values + /- s.e.m.) for tumor growth and mean values + /- s.d. for tumor weight. **** p < 0.0001 (two-sided t-test).
