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Fig. 11 | Journal of Experimental & Clinical Cancer Research

Fig. 11

From: YAP transcriptionally regulates COX-2 expression and GCCSysm-4 (G-4), a dual YAP/COX-2 inhibitor, overcomes drug resistance in colorectal cancer

Fig. 11

YAP and COX-2 were essential for the effect of G-4 (10 μM) and acted synergistically to overcome the resistance. a Western blot analysis of YAP and COX-2 in YAP or COX-2 expressing vector-transfected HCT15/Tax cells treated with G-4 (10 μM) for 48 h. **P < 0.01 compared with G-4. b Flow cytometric analysis for apoptosis

in YAP or COX-2 expressing vector-transfected cells treated with G-4 (10 μM) for 48 h. Left panel: HCT8/Tax cells; right panel: HCT15/Tax cells. **P < 0.01 compared with G-4. c Apoptosis and cell viability of HCT15/Tax cells treated with Taxol, Taxol plus Verteporfin (T + V), Taxol plus Celecoxib (T + C), Taxol plus G-4 (T + G) respectively for 48 h. **P < 0.01 compared with Taxol, ## P < 0.01 compared with T + V, && P < 0.01 compared with T + C. (Taxol: 1 μM; Verteporfin, Celecoxib, G-4 are all 10 μM). d YAP or COX-2 expression after shRNA transfection for different time (upper panel), and western blot of YAP and COX-2 (lower panel) after 48 h shYAP or shCOX-2 transfection in HCT15/Tax cells. *P < 0.05, **P < 0.01 compared with control. e Apoptosis and cell viability of HCT15/Tax cells after shYAP or shCOX-2 was introduced. **P < 0.01 compared with Taxol, ## P < 0.01 compared with shYAP, && P < 0.01 compared with shCOX-2. All data are representative of at least three independent experiments. Error bars represent SD. Tax: Taxol, VP: verteporfin, Cel: celecoxib, G-4: GCCSysm-4.

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