Fig. 5

FFA1-mediated pRCC cell proliferation is regulated by AKT, NF-κB, and COX-2. A FFA1 agonism increased the expression of the p65 subunit of NF-κB compared to vehicle-treated control. The graphical results shown are representative of four independent experiments quantifying the p65 subunit. B FFA1 agonism increased the expression of COX-2 compared to vehicle-treated control. The graphical results shown are representative of four independent experiments quantifying COX-2. Statistical significance was determined by paired t-test. * denotes p < 0.05, **denotes p < 0.01, and *** denotes p < 0.001 versus the control condition. C MK2206 (1 µM) significantly decreases FFA1-mediated cell proliferation (p < 0.01; d = 8.35, versus AS2034178). When used alone, MK2206 inhibited serum-induced cell proliferation compared to control condition (p < 0.01; d = 3.25, versus control). D BAY 11-7082 (1 µM) significantly inhibited cell proliferation in the presence of AS2034178 (p < 0.01; d = 5.56, versus AS2034178). Compared to the vehicle-treated control condition, BAY 11-7082 suppressed serum-induced pRCC cell proliferation (p < 0.05; d = 2.90, versus control). E Celecoxib decreases FFA1-mediated cell proliferation (p < 0.001; d = 6.70, versus AS2034178). Statistical significance was determined by paired t-test. Graphs depict combined replicate data from four independent experiments each performed in triplicate. *denotes p < 0.05, and ** denotes p < 0.01 versus the control condition, while ## denotes p < 0.01, and ### denotes p< 0.001 versus the AS2034178-treated condition