Fig. 3From: YAP transcriptionally regulates COX-2 expression and GCCSysm-4 (G-4), a dual YAP/COX-2 inhibitor, overcomes drug resistance in colorectal cancerYAP increases COX-2 transcription through intact TEAD response elements. a Transfection of COX-2 luciferase promoter reporter into SW480 cells with or without YAP plasmids. COX-2 luciferase reporter activity was measured after 48Â h. b Co-transfection of COX-2 luciferase promoter reporter with YAP or YAP plus TEAD into 293Â T cells; COX-2 luciferase reporter activity was detected after 48Â h. **PÂ <Â 0.01 compared with control cells. c Wide type TEAD response elements and deletion of the TEAD response elements were described. Sequence of the COX-2 promoter and two binding sites were identified (bold/underlined, upper panel). Co-transfection of COX-2 luciferase promoters (wide type or deleted in the TEAD binding sites, middle) with YAP or control vector into 293Â T cells; COX-2 luciferase reporter activity was detected after 48Â h (lower panel). d COX-2 luciferase reporter activity (wide type or deleted in the TEAD response elements) was detected after 48Â h in HCT-116 cells. e mRNA levels of COX-2 were determined by qRT-PCR in HCT-116 cells of d. **PÂ <Â 0.01 compared with WT, ## PÂ <Â 0.01 compared with Del1 or Del2. f ChIP analysis of YAP interaction with the COX-2 promoter in vivo. **PÂ <Â 0.01 compared with SW480. Data are representative of at least three independent experiments. Error bars represent SDBack to article page