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Fig. 5 | Cell Communication and Signaling

Fig. 5

From: NF-κB potentiates tumor growth by suppressing a novel target LPTS

Fig. 5

HPV16-E6 promotes NF-κB-dependent growth of CaSki cells. a HPV16-E6 stimulates the activity of NF-κB. The empty vector or pEGFP-HPV16-E6-transfected CaSki cells were additionally transfected with a reporter gene which contains consensus binding elements of NF-κB, and then treated with a NF-κB inhibitor BAY11–7082 (10 μM) for 24 h. Cells were then harvested for luciferase activity assays (n = 4, **P < 0.01, means ± s.e.ms., Student’s t-test). b EMSA was conducted to examine the binding activity between p65 and probe 1 which contains a potential NF-κB binding site locating at −888/−881 in the promoter of human LPTS. The cell lysates were collected from the empty vector or HPV16-E6-transfected CaSki cells. Representative results were displayed. c Relative mRNA expression of LPTS in the empty vector or HPV16-E6-transfected CaSki cells which were treated with DMSO or a NF-κB inhibitor BAY11–7082 (10 μM) for 24 h. (n = 4, **P < 0.01, means ± s.e.ms., Student’s t-test). d Immunoblotting assays of LPTS and p-65 proteins in the cells as described in (c). e CCK8 assays of the CaSki cells. The empty vector or HPV16-E6-transfected CaSki cells were treated with DMSO or a NF-κB inhibitor BAY11–7082 (10 μM). CCK8 assays were performed dynamically as indicated (n = 5, **P < 0.01, means ± s.e.ms., Student’s t-test). f Volume of the inoculated CaSki tumors. The empty vector or HPV16-E6-transfected CaSki cells were inoculated subcutaneously in the Balb/C nude mice and treated with DMSO or a NF-κB inhibitor BAY11–7082 every three days. The tumor size was measured dynamically (n = 5, *P < 0.05, means ± s.e.ms., Student’s t-test)

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