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An Oncogenic Hepatocyte-Induced Orthotopic Mouse Model of Hepatocellular Cancer Arising in the Setting of Hepatic Inflammation and Fibrosis
Published on: September 12, 2019
Decoy receptor 3 overexpression and immunologic tolerance in hepatocellular carcinoma (HCC) development
Caixia Chen1, Changgong Zhang, Guohong Zhuang
1Anti-Cancer Research Center, Xiamen University Medical College, XiaMen, China.
Abstract:
The recently identified decoy receptor 3 (DcR3) inhibits FasL-induced apoptosis by binding to FasL, and it is considered to play a key role in the immune escape system of neoplastic cells. In order to examine the involvement of DcR3 in the immunologic tolerance of hepatocellular carcinoma (HCC), we investigated the amplification and expression of DcR3, FasL, and Fas in an HCC mice model using RT-PCR, western blotting, and ELISA, and analyzed the space-time relationship with various cytokines including the forkhead transcription factor forkhead/winged helix transcription factor gene (Foxp3), CTLA-4, TGF-beta, IL-10, TNF-alpha, and IFN-gamma. The RT-PCR results revealed that Fas expression preceded that of DcR3 during the early phases of tumorigenesis. Thereafter, the expression of DcR3 was up-regulated; however, the expression of Fas was down-regulated and eventually ceased. DcR3 and FasL were expressed and amplified simultaneously in muscle tumor. CTLA-4 expression was earlier than Foxp3, and both CTLA-4 and Foxp3 amplification and expression were consistent with that of DcR3. The results suggest that the elevated levels of DcR3, Foxp3, and CTLA-4 in tissue were positively correlated with tumor growth. The partial tumor immunoregulation inclined to negative modulation, and DcR3 may play an important role in inducing immunologic tolerance.
Insights
Decoy receptor 3 (DcR3) is upregulated in hepatocellular carcinoma (HCC), suppressing immune responses and promoting tumor growth. This study reveals DcR3
Area of Science:
- Immunology
- Oncology
- Molecular Biology
Background:
- Decoy receptor 3 (DcR3) is identified as a key factor in neoplastic immune evasion by inhibiting FasL-induced apoptosis.
- Hepatocellular carcinoma (HCC) is a significant malignancy where immune tolerance mechanisms are crucial for tumor progression.
Purpose of the Study:
- To investigate the role of DcR3 in the immunologic tolerance of HCC.
- To analyze the temporal expression patterns of DcR3, FasL, Fas, and related immune cytokines in an HCC mouse model.
Main Methods:
- Real-time quantitative PCR (RT-PCR) to assess gene amplification and expression.
- Western blotting and Enzyme-Linked Immunosorbent Assay (ELISA) for protein level analysis.
- Analysis of cytokines including Foxp3, CTLA-4, TGF-beta, IL-10, TNF-alpha, and IFN-gamma.
Main Results:
- Fas expression initially preceded DcR3 during early tumorigenesis, followed by DcR3 upregulation and Fas downregulation.
- Simultaneous expression and amplification of DcR3 and FasL were observed in muscle tumors.
- Elevated DcR3, Foxp3, and CTLA-4 levels correlated positively with tumor growth, indicating a shift towards negative immunoregulation.
Conclusions:
- DcR3 plays a significant role in inducing immunologic tolerance in HCC.
- The findings suggest DcR3 contributes to tumor immune escape and progression.
- Targeting DcR3 may represent a potential therapeutic strategy for HCC.
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