ERK inhibitor SCH772984 is insensitive to overexpression of either CK2α(WT) or CK2α(K68M).
A, the GI50 for ERKi SCH772984 is unchanged by overexpression of CK2α or by mutant NRAS. GI50 curves were generated after 72 h of ERKi treatment. Results are presented as means ± S.E. (n = 3). B, clonogenic survival in the presence of ERKi is not enhanced by overexpressed CK2α or mutant NRAS. Shown are the percentages of colonies formed by A375 cells expressing GFP, CK2α, or NRAS(Q61K) and treated with ERKi (100 nm) normalized to DMSO vehicle control. Results are presented as means ± S.E. (n = 3). n.s., non-significant compared with GFP. C, ERKi treatment shuts down ERK pathway signaling as indicated by loss of phosphorylated ERK substrate pRSK. A375 cells as in A and B were treated for 24, 48, or 72 h with 100 nm SCH772984. Error bars represent S.E. tERK, total ERK; tRSK, total RSK.