Fig. 6
NF-κB activation mediates XPR1-mediated oncogenic effects. (a-c) XPR1-overexpressing SCC-25 and CAL-27 cells were transfected with IκB-α-mut or treated with NF-κB inhibitor QNZ at 10 nM for 24 h, and then applied for colony formation assay (a), transwell penetration assay (b), and annnexin V/PI assay (c). (d) 5 × 106 vector control, XPR1-overexpressing, or XRP1 and IκB-α-mut-overexpressing SCC-25 cells were subcutaneously injected into Balb/c nude mice and inocubated for 6 weeks. Tumors in each group were shown. (e) Tumor volumes were calculated weekly. (f) Tumor weights in each group. (g) IHC staining of XPR1 and Ki67, as well as TUNEL staining in xenograft section. Proliferation index was indicated by Ki67-positive cell percentage. Apoptotic index was calculated by the percentage of TUNEL-positive cells. (h) Clinical relevace of XPR1 expression and NF-κB activation in patient specimens. Representative images of XPR1 and p65 IHC staining in 128 TSCC patient specimens. Correlation analysis revealed that high expression of XPR1 significantly associated with nuclear p65 expression. χ2 test was used. **P < 0.01, ***P < 0.001