CXCR4 and lip and oral cavity carcinoma: Moreover, NF-κB inhibitor PDTC was then used in Cal 27 cells treated with pDC-CM, and resulted in no significantly change of CXCR-4 expression, NF-kB activation (Figure 5C,D), cancer cell proliferation (Figure 5E,F) and invasion (Figure 6A,B), suggesting that pDC-CM-mediated CXCR-4 overexpression in oral cancer Cal 27 cells occurs, in part, through the NF-κB pathway.