Figure S1: Validation of tumor resistance mutations of EZH2. Figure S2: RB1del cells show morphological and transcriptional responses to TAZ. Figure S3: TAZ-treated RB1del cells show evidence of differentiation at the transcript, but not protein level. Figure S4: RB1del cells show increased expression of E2F targets. Figure S5: Characterization of MRT and ES cell lines. Figure S6: Generating and testing CDKN1Adel and CDKN2Adel G401 cells. Figure S7: TAZ-resistant patient tumors show upregulation of cell cycle genes. Figure S8: Transcriptomic analysis of patient tumors nominates putative biomarkers of TAZ sensitivity and resistance. Figure S9: Downstream cell cycle inhibitors overcome resistance to TAZ. Figure S10: TAZ + barasertib increases cell cycle arrest without inducing apoptosis. Figure S11: p16 induction correlates with TAZ response in vivo. Figure S12: Induction of immune-related genes and endogenous transposable elements by TAZ. Figure S13: TAZ may remodel BAF and PRC2 composition by transcriptional regulation of their subunits.
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Kazansky et al. (2024) studied this question.
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