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. Author manuscript; available in PMC: 2021 Jun 1.
Published in final edited form as: Cancer Prev Res (Phila). 2020 Sep 11;13(12):979–988. doi: 10.1158/1940-6207.CAPR-20-0186

Figure 4. Genetic disruption of EZH2 catalytic activity attenuates MYC driven HG-PIN.

Figure 4.

(A) Representative dorso-lateral H&E images and pathological assessment from mice treated with vehicle control or tamoxifen (1mg, days 1–5) attenuates the occurrence of MYC driven HG-PIN. (D) Immunohistochemical staining demonstrates the genetic inhibition of EZH2 catalytic activity reduces tumor positivity for EZH2 and H3K27me3 expression. Tumor cell proliferation is attenuate as indicated by reduction in Ki67 expression. Scale bar = 200μm. (C) Organoids generated from our genetically engineered mouse model had EZH2 catalytic activity inhibited by chemical (DMSO verse EPZ6438, 10μM day 0 and day 3) or genetic (AdCtl or AdCre) methods. Results for (C) represent the mean of 3 independent experiments ± SEM. Multiple T-test analysis demonstrates that EZH2 catalytic inhibition significantly attenuates prostate cancer organoid generation driven by MYC. **p<0.0001.