Fig. 4
From: SWI/SNF catalytic subunits’ switch drives resistance to EZH2 inhibitors in ARID1A-mutated cells
ABT263 overcomes de novo resistance to the EZH2 inhibitor. a, b Parental and resistant TOV21G cells were treated with 0.5 μM ABT263, 5 μM GSK126, or in combination. Expression of markers of apoptosis were analyzed by immunoblot (a) or quantified by Annexin V staining (b). c Synergy analysis between GSK126 and ABT263 in TOV21G cells. d–f ABT263 regresses the established EZH2 inhibitor-resistant TOV21G orthotopically transplanted tumors (d, e) and improves the survival of the tumor-bearing mice (f) in vivo. g GSK126 and ABT263 are synergistic in suppressing the growth of the xenograft ovarian tumors formed by primary OCCC cultures. h, i Immunohistochemical staining for EZH2, H3K27me3, Ki67, and cleaved caspase 3 using consecutive sections of the dissected tumors from the indicated treatment groups (h). Bar = 100 μM. Histological score (H score) calculated for the indicated staining (i). Data represent mean ± S.E.M. of three independent experiments (a–c). P-value was calculated via two-tailed t-test
