Related Experiment Video
Updated: Apr 19, 2026

Author Spotlight: Comparing Alveolar and Long Bone Remodeling to Explore OTM Model Potential
Published on: July 21, 2023
14-3-3ζ regulates immune response through Stat3 signaling in oral squamous cell carcinoma
Xinguang Han1, Yongfu Han1, Huifeng Jiao1
1Department of Oral and Maxillofacial Surgery, the First Affiliated Hospital, Zhengzhou University, Zhengzhou 450052, China.
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.
Insights
14-3-3ζ protein is overexpressed in oral squamous cell carcinoma (OSCC), promoting tumor inflammation and immune evasion. This protein regulates immune cell responses and inflammation via Stat3 signaling in OSCC.
Area of Science:
- Oncology
- Immunology
- Molecular Biology
Background:
- Ectopic 14-3-3ζ expression is observed in multiple cancers.
- The role of 14-3-3ζ in tumor-immune interactions remains unexplored.
Purpose of the Study:
- Investigate 14-3-3ζ's role in modulating tumor inflammation.
- Determine 14-3-3ζ's involvement in immune recognition evasion in oral squamous cell carcinoma (OSCC).
Main Methods:
- Analyzed 14-3-3ζ expression in OSCC cell lines and tissues.
- Performed 14-3-3ζ knockdown and introduction experiments.
- Assessed cytokine expression and immune cell responses.
- Investigated the interaction between 14-3-3ζ and Stat3 signaling.
Main Results:
- 14-3-3ζ is overexpressed in OSCC.
- Knockdown of 14-3-3ζ up-regulated inflammatory cytokines in OSCC cells.
- 14-3-3ζ introduction attenuated cytokine expression in normal cells.
- 14-3-3ζ affected peritoneal macrophages, dendritic cells, and T cells.
- Stat3 directly interacts with 14-3-3ζ, mediating its effects on inflammation.
Conclusions:
- 14-3-3ζ plays a significant role in regulating tumor inflammation in OSCC.
- 14-3-3ζ contributes to immune evasion in OSCC.
- Stat3 signaling is a key pathway through which 14-3-3ζ influences tumor inflammation and immune response.
Related Concept Videos
Receptor Downregulation in MVBs
The EGFR can initiate signaling pathways that lead to cell proliferation, migration, and differentiation. Overexpression of EGFR stimulates cells to proliferate. Excessive EGFR...
The JAK-STAT Signaling Pathway
Role Of Notch Signalling In Intestinal Stem Cell Renewal
Direct cell-to-cell contact is needed for the activation of Notch signaling. The signal is initiated when a notch ligand binds to a receptor on an adjacent cell, also...
Abnormal Proliferation
Regulation of Hematopoietic Stem Cells

