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. Author manuscript; available in PMC: 2019 Jun 1.
Published in final edited form as: Clin Cancer Res. 2018 Mar 7;24(11):2616–2630. doi: 10.1158/1078-0432.CCR-17-1207

Figure 6. Pharmacologic inhibition of TAZ-TEAD activity diminishes aRMS cell and tumor growth.

Figure 6.

TEAD luciferase activity (8XGTIIC–Luc reporter) is (A) increased in Rh28 cells expressing constitutively activate TAZ mutant TAZS89A, but partially reversible with treatment of 10μM VP, (B) decreased in Rh28 cells treated with 10μM VP, as well as in Rh28 cells stably expressing TAZ shRNAS; and (C) decreased in Rh28 cells treated with 1μM or 10μM PPIX. (D, E) Dose response curve in Rh28 cells treated with VP or PPIX. (F) Rh28 cells treated with 10μM PPIX have decreased cell growth, as measured by manual cell counting. (G) Rh28 xenografts treated with 100mg/kg VP have decreased tumor growth as compared to vehicle control (DMSO). (H) TAZS89A decreases Rh28 cell sensitivity to VCR. (I) Dose-dependent cooperativity with either 0.3μM or 1μM VP and VCR in Rh28 cells. (J) The combination of VP and VCR in vivo is more effective than either agent alone in inhibiting tumor growth. N = 5 mice in each group. VP, verteporfin; PPIX, protoporphyrin IX.