Fig. 7: ERK-MYD88 interaction inhibition by EI-52 induces cancer cell death and immune T-cell response in vivo.
From: Targeting ERK-MYD88 interaction leads to ERK dysregulation and immunogenic cancer cell death
Following s.c. implantation of syngeneic CT26 cells, BALB/c mice were treated intraperitoneally for 24 h with vehicle or 50 mg/kg of EI-52 and tumors were collected. A Cleaved-PARP was observed by IHC staining, representative of four separate mice or (B) by western Blot of tumor cell lysates recovered from four mice per treatment. C Following s.c. implantation of CT26 cells, syngeneic wild-type and nude BALB/c mice (n = 10/group) were treated daily with vehicle or with 25 mg/kg of EI-52 intraperitoneally. Tumor volume was measured twice a week with an electronic caliper. Results are presented as Mean tumor volume ± SEM, Sidak’s two-way ANOVA, Balb/c day 14 Vehicle/vs EI-52 ****p < 0,0001 (95% confidence interval). D Following s.c. implantation of CT26 cells, mice (n = 10/group) were treated daily with vehicle or with 25 mg/kg of EI-52 intraperitoneally. At days 0, 3, and 5, mice received an intraperitoneal injection of 200 μg isotype control or anti-PD1 antibody. Tumor volume was measured twice a week with an electronic caliper. Results are presented as Mean tumor volume ± SEM, Tukey’s two-way ANOVA, day 14 Vehicle/isotype control vs EI-52/isotype control *p = 0.0115, EI-52/isotype control vs EI-52/anti-PD1 *p = 0.0335 (95% confidence interval). Source data are provided as a Source Data file.
