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. 2016 Sep 22;7(45):73032–73044. doi: 10.18632/oncotarget.12195

Figure 2. Activation of NFκB in MEC.

Figure 2

(A) NFκB (p65) (yellow arrows) was significantly increased in the nucleus of MEC samples compared to normal salivary glands, which showed prevalent cytoplasmic staining (arrowhead) (***p < 0.001, n = 11, mean ± SD). (B) Immunofluorescence of UM-HMC-3A, UM-HMC-3B, and UM-HMC-5 tumor cell lines depict the presence of nuclear NFκB (yellow arrows). (C) UM-HMC-3A, UM-HMC-3B, and UM-HMC-5 show detectable NFκB (p65) protein levels at baseline (0 Gy). NFκB is increased in UM-HMC-5 following 2 Gy of IR (*p < 0.05, mean ± SD from experiments run in triplicate). (D) Clonogenic assay for MEC cells with no stimuli or TNF-α stimuli revealed that NFκB upregulation significantly increases the resistance of UM-HMC-3A and UM-HMC-3B (**p < 0.01, ***p < 0.001, n = 3, mean ± SD compared to 0 Gy). (E) Western blot of UM-HMC-3A, UM-HMC-3B, and UM-HMC-5 for phosphorylated p53 (ser15) depict high expression of the p53 protein on UM-HMC-5 cells. UM-HMC-3A and 3B are absent of p53 protein levels.