AI Article Synopsis
- Ectopic expression of the protein 14-3-3ζ is found in various cancers, including oral squamous cell carcinoma (OSCC), but its role in tumor-immune system interactions has not been previously studied.
- 14-3-3ζ knockdown in OSCC cells increased the expression of inflammatory cytokines, while introducing 14-3-3ζ decreased these cytokines in normal cells stimulated by inflammatory agents.
- The protein 14-3-3ζ interacts with Stat3, and disrupting this interaction alleviates the inhibitory effects of 14-3-3ζ on tumor inflammation, suggesting it may play a crucial role in modulating tumor inflammation and the immune response in OSCC.
Article Abstract
Ectopic expression of 14-3-3ζ 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 14-3-3ζ 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 14-3-3ζ is implicated in tumor inflammation modulation and immune recognition evasion. In oral squamous cell carcinoma (OSCC) cell lines and cancer tissues, we found that 14-3-3ζ is overexpressed. In OSCC cells, 14-3-3ζ knockdown resulted in the up-regulated expression of inflammatory cytokines. In contrast, 14-3-3ζ introduction attenuated cytokine expression in human normal keratinocytes and fibroblasts stimulated with interferon-γ (IFN-γ) and lipopolysaccharide (LPS). Furthermore, supernatants from 14-3-3ζ 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 14-3-3ζ and its disruption relieved the inhibition induced by 14-3-3ζ in tumor inflammation. Taken together, our studies provide evidence that 14-3-3ζ may regulate tumor inflammation and immune response through Stat3 signaling in OSCC.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4332029 | PMC |
| http://dx.doi.org/10.14348/molcells.2015.2101 | DOI Listing |
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