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. 2018 Mar 17;20(4):401–409. doi: 10.1016/j.neo.2018.01.012

Figure 4.

Figure 4

CEACAM1 expression is controlled by the MAPK pathway via the ETS1 transcription factor.

(A) CEACAM1 promoter with a deletion in the putative ETS1 binding site on the negative strand (delETS1(−)), positive strand (delETS1(+)), or the wild-type sequence (WT) was cloned upstream to firefly luciferase and co-transfected into the indicated melanoma cell lines together with a normalizing construct of Renilla luciferase. Empty vector served as negative control. Cells were treated for 2 days with DMSO, or 1 μM vemurafenib (VEM) or selumetinib (SEL). Relative promoter activity was calculated relative to the control (cells transfected with an empty vector and treated with DMSO). Figure shows the average results of four independent experiments. (B) ETS1 expression in the indicated melanoma lines in the presence or absence of vemurafenib. Figure shows a representative experiment out of four independent experiments. Significance was tested with ANOVA, * depicts P value of <.05.