摘要Background A20, also known as tumor necrosis factor α induced protein 3 (TNFaip3), is a cytoplasmic zinc finger protein that inhibits nuclear factor kappa-B (NF-κB) activity and prevents tumor necrosis factor (TNF)-mediated programmed cell death. NF-κB is a transcription factor that regulates expression of genes involved in cell proliferation,cell survival and anti-apoptosis. Several studies have implicated that the NF-κB signal pathway is associated with angiogenesis and clinico-pathological process of adenoid cystic carcinoma (ACC) of the salivary glands.Methods The ability of overexpression of A20 to influence the biological behavior and invasion of ACC cells was examined. The cells were stably transfected with full-length A20 cDNA. Stable gene transfer was verified by realtime-polymerase chain reaction (PCR) and Western blot analysis. The change of cell biological behavior was examined by methyl thiazolyl tetrazolium (MTT) and NF-κB luciferase reporter assay and the invasion of the cells was examined by a Matrigel invasion chamber.Results pEGPFN3-A20 gene was stably transferred into ACC-2 cells and overexpressed. When cells were treated with TNFα, the NF-κB activity of ACC-2-A20 cells could be down-regulated about 46.32% in contrast to ACC-2-GFP cells (P＜0.05). A20 potently inhibited growth of A20 transfectant ACC-2-A20 compared with control vector transfected groups and the ACC-2 empty control group (P＜0.05). The ACC-2-A20 cells showed significantly reduced ability to invade through Matrigei-coated filters compared to ACC-2-GFP and ACC-2 cells. The inhibition rate was up to 71.05% (P＜0.05).Conclusions A20 gene transfer is associated with decreased tumor invasion, in part via the down-regulation of NF-κB expression, providing evidence for a potential application of A20 in designing a treatment modality for salivary gland cancers such as ACC.