Human beta-defensin 3 contributes to the carcinogenesis of cervical cancer via activation of NF-κB signaling.

Human beta-defensin 3 (hBD3), an antimicrobial peptide (AMP) expressed in epithelium in response to various stimulations including human papillomavirus infection, has recently been found to be overexpressed in head and neck cancers and exhibit tumorigenic activities. However, the role of hBD3 in cervical cancer remains to be investigated. In this study, we showed by immunohistochemistry that hBD3 expression was elevated in cervical cancer samples of different stages versus the normal tissue, and was positively correlated with the progression of the disease. Overexpression of hBD3 in cervical cancer cell lines promoted cell proliferation by accelerating G1/S progression and enhanced cell migration and invasion in vitro. These oncogenic effects of hBD3 were associated with activation of NF-κB signaling. Using a mouse xenograft model, we further demonstrated that hBD3 overexpression promoted the growth of cervical cancer cells in vivo. Our results suggested that hBD3 is involved in the carcinogenesis and development of cervical cancer, and may serve as a biomarker or therapeutic target of this disease.