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. 2015 Sep 29;16(11):1660–1670. doi: 10.1080/15384047.2015.1099769

Figure 5.

Figure 5.

Ovarian tumor cell killing requires activation of the JNK pathway and inactivation of [STAT3 + AKT + NFκB]. (A) Spiky ovarian tumor cells were treated with vehicle; [sorafenib (2 μM) + sildenafil (2 μM)]; [celecoxib (2 μM) + sildenafil (2 μM)]; or all 3 drugs together for 6h. Six h after drug treatment, cells were fixed in place and immuo-staining performed to detect the phosphorylation of JNK1/2; STAT3; STAT5; AKT T308; p65 NFκB; and ERK1/2, using a Hermes WiScan wide field microscope. (B) OVCAR and Spiky cells were transfected with empty vector plasmid (CMV) or plasmids to express activated MEK1; activated AKT; activated STAT3; and the dominant negative super-repressor IκB S32A S36A. A portion of CMV transfected cells was treated with the JNK inhibitory peptide (10 μM). Twenty four h after transfection, cells were treated with vehicle; [sorafenib (2 μM) + sildenafil (2 μM)]; [celecoxib (2 μM) + sildenafil (2 μM)]; or all 3 drugs together for 24h. Twenty four h after drug treatment, cells were processed and subjected to live/dead assays in a Hermes Wiscan system.