Skip to main content
. 2021 Jan 19;12(2):66–80. doi: 10.18632/oncotarget.27868

Figure 5. MEK inhibition enhances the anti-tumor effect with TA99 mAb.

Figure 5

B16 cells were treated with MEKi for the indicated times and protein lysates were subjected to western blot analysis. MEK inhibition (as shown by dephosphorylation of ERK) resulted in increased levels of TYRP1 and MITF (A) and increased pigmentation (B). Trametinib also induced increased levels of TYRP1 in BRAFV600E-mutant YUMM cells (C). RNA was prepared after treatment with trametinib, and increased expression of different melanosomal antigens was observed by qRT-PCR analyses. Relative expression of melanosomal antigens from technical triplicates is shown. Grey bars represent DMSO-treated controls, and blue bars represent melanoma cells after treatment with trametinib. Melanosomal antigens measured are: MART, MITF, GPR143, PMEL, TYR, GPMNB, DCT and TYRP1 (D) * p < 0.05; ** p < 0.001; *** p < 0.0001. Combined treatment with trametinib and TA99 (E) resulted in an enhanced anti-melanoma effect in both B16 and YUMM1.9 subcutaneous tumors in C57BL/6 mice (F). Differences in tumor growth were determined by two-way ANOVA with Bonferroni correction (n = 5 mice per group). * p < 0.05; ** p < 0.001. Comparison between the corresponding treatment group and the untreated control is shown.