| 초록 |
Ectopic expression of $14-3-3{ zeta}$ has been found in various malignancies, including lung cancer, liver cancer, head and neck squamous cell carcinoma (HNSCC), and so on. However, the effect of $14-3-3{ zeta}$ in the regulation of interactions between tumor cells and the immune system has not been previously reported. In this study, we aimed to investigate whether and how $14-3-3{ zeta}$ is implicated in tumor inflammation modulation and immune recognition evasion. In oral squamous cell carcinoma (OSCC) cell lines and cancer tissues, we found that $14-3-3{ zeta}$ is overexpressed. In OSCC cells, $14-3-3{ zeta}$ knockdown resulted in the up-regulated expression of inflammatory cytokines. In contrast, $14-3-3{ zeta}$ introduction attenuated cytokine expression in human normal keratinocytes and fibroblasts stimulated with interferon- ${ gamma}$ (IFN- ${ gamma}$ ) and lipopolysaccharide (LPS). Furthermore, supernatants from $14-3-3{ zeta}$ knockdown OSCC cells dramatically altered the response of peritoneal macrophages, dendritic cells and tumor-specific T cells. Interestingly, Stat3 was found to directly interact with $14-3-3{ zeta}$ and its disruption relieved the inhibition induced by $14-3-3{ zeta}$ in tumor inflammation. Taken together, our studies provide evidence that $14-3-3{ zeta}$ may regulate tumor inflammation and immune response through Stat3 signaling in OSCC. |
