Fig. 6: β-catenin co-factors as actionable targets against resistance. | Cell Death & Differentiation

Fig. 6: β-catenin co-factors as actionable targets against resistance.

From: Role of the cross-regulation between Wnt pathway activation and androgen receptor signaling in prostate cancer treatment resistance

Fig. 6: β-catenin co-factors as actionable targets against resistance.

A TCF reporter activity on PC3 cells expressing β-catenin mutant variants I. T41A or II. D32G under IQ-1 or ICG-001 treatment (2, 5 or 10 µM, 24 H. DMSO as vehicle). B AXIN2, RNF43, ZNRF3, and NKD1 (top Wnt signature genes) expression evaluated by RT-qPCR in PC3 cells expressing β-catenin D32G mutant variant treated with IQ-1 or ICG-001 (2 or 5 µM, 24 H. DMSO as vehicle). C TCF reporter activity from I. C42B and II. LNCaP cells expressing β-catenin T41A and D32G mutant variants, respectively, under enzalutamide treatment (30 µM, 24 H) combined or not combined with IQ-1 or ICG-001 (2, 5, or 10 µM, 24 H. DMSO as vehicle). D Expression of AXIN2, RNF43, ZNRF3, and NKD1 (top Wnt signature genes) evaluated by RT-qPCR in I. C42B and II. LNCaP cells expressing β-catenin T41A and D32G mutant variants, respectively, treated with enzalutamide (30 µM, 24 H) combined or not combined with IQ-1 or ICG-001 (2, 5, or 10 µM, 24 H. DMSO as vehicle). E CellTiter-Glo® Cell Viability Assay of I. C42B and II. LNCaP cells expressing β-catenin T41A and D32G mutant variants, respectively, under enzalutamide treatment (30 µM, 24 H) combined or not combined with IQ-1 or ICG-001 (2, 5, or 10 µM, 72 H). DMSO as vehicle). F CellTiter-Glo® 3D Cell Viability Assay of organoids derived from MDA PCa 173-2 treated with enzalutamide (0–150 µM), combined or not combined with I. IQ-1 or II. ICG-001 (2, 5, or 10 µM) (72 H; DMSO as vehicle). Statistical significance was assessed by one-way ANOVA or non-linear regression comparison. Statistical significance: * P < 0.05; ** P < 0.01; *** P < 0.001.

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