Human β-defensin-3 and nuclear factor-kappa B p65 synergistically promote the cell proliferation and invasion of oral squamous cell carcinoma

Background: Oral squamous cell carcinoma (OSCC) is a usual oral cancer; it’s necessary to identify targets for its early diagnosis and treatment. This research aimed to investigate the roles of human β-defensin-3 (hBD-3) and nuclear factor-kappa B (NF-κB) p65 in the pathogenesis and progression of OSCC. Methods: : The connection between NF-κB p65 and the carcinogenesis of oral cancer was explored by immunohistochemical staining. The relative expressions of hBD-3 and NF-κB p65 in OSCC cells were evaluated by qRT-PCR and Western blot. Afterwards, hBD-3 was knocked down, and NF-κB p65 was overexpressed. The cell viability and invasion were tested via CCK-8 and Transwell experiment, and the expression of hBD-3, NF-κB p65 and its downstream molecules were evaluated by Western blot. Results: : The content of NF-κB p65 was increased with the aggravation of oral submucosal fibrosis. hBD-3 and NF-κB p65 were high-expressed in OSCC cells. The viability and invasion abilities of OSCC cells that knocking down hBD-3 were markedly decreased, while they were restored by co-overexpression of NF-κB p65. The expressions of NF-κB p65, c-myc were decreased and IκB, p21 were increased with the knockdown of hBD-3. After co-overexpression of NF-κB p65, the expression of hBD-3 and IκB didn’t change significantly, while c-myc and p21 was dramatically changed. Conclusion: hBD-3 and NF-κB p65 facilitate the proliferation and invasion of OSCC cells, and hBD-3 may promote this process by regulating the expression of NF-κB p65 and its downstream c-myc and p21.