Figure 6 from MYBL2 Drives Prostate Cancer Plasticity: Inhibiting Its Transcriptional Target CDK2 for RB1-Deficient Neuroendocrine Prostate Cancer

Inhibition of CDK2 represents a novel therapeutic target for NEPC. A, Tumoral growth curve of murine DKO cells in C57BL/6N and (B) PPKO cells in C57BL/6N mice and treated with either vehicle control or the CDK2 PROTAC—CPS2. Mice were treated every 7 days (D7 and D14) with CPS2 (400 mg/kg) by intraperitoneal injection. Tumor growth was monitored every second day for 16 days (D16) by serial caliper measurements. Tumoral weight was measured at D16 after dissection (n = 5 mice per treatment group (±1 SEM). C, Immunofluorescent IHC staining for CDK2 in DKO and (D) PPKO tumors show that CPS2 inhibition significantly reduces CDK2 expression. E and F, Example pictures of hematoxylin and eosin, Ki67, and p-γH2AX IHC staining in murine DKO and PPKO tumors from the in vivo study and corresponding quantification of the percentage of positive nuclei from total cells (n = 5 mice per treatment group, ±1 SEM).