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Publications (5)2.08 Total impact

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    ABSTRACT: The INK4b-ARF-INK4a gene cluster encodes three tumor suppressors: p15(INK4b), p14(ARF), and p16(INK4a). Antisense non-coding RNA in the INK4 locus (ANRIL) is transcribed in the opposite direction from this gene cluster. Recent studies suggest that ANRIL represses the expression of p15(INK4b), p14(ARF), and p16(INK4a); however, the underlying mechanism is unclear. In this study, the expressions of ANRIL in human esophageal squamous cell carcinoma (ESCC) tissues and matched adjacent non-tumor tissues were examined by quantitative real-time polymerase chain reaction. Compared with matched adjacent non-tumor tissues, the expression levels of ANRIL in ESCC tissues were significantly increased. Furthermore, inhibition of ANRIL was found to increase the expression of p15(INK4b) and transforming growth factor β1 (TGFβ1) and depletion of ANRIL in ESCC cell lines may inhibit cellular proliferation. Thus, our findings suggest a significant role of ANRIL in the occurrence and development of ESCC through TGFβ1 signaling pathways.
    Cellular Immunology 04/2014; 289(1-2):91-96. · 1.74 Impact Factor
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    ABSTRACT: Human γδ T cells display the principal characteristics of professional antigen-presenting cells (APCs), in addition to playing a vital role in immunity through cytokine secretion and their cytotoxic activity. However, it is not clear whether γδ T cells perform APC-like functions under pathological conditions. In this study, we showed that, in contrast to peripheral-derived γδ T cells directly isolated from PBMCs of gastric cancer patients, tumor-activated γδ T cells not only killed tumor cells efficiently but also strongly induced primary CD4(+) and CD8(+) αβ T cells proliferation and differentiation. More importantly, they abrogated the immunosuppression induced by CD4(+)CD25(+) Treg cells and induced the cytotoxic function of CD8(+) αβ T cells from patients with gastric cancer. In conclusion, tumor-activated γδ T cells can induce adaptive immune responses through their APC-like functions, and these cells may be a potentially useful tool in the development of tumor vaccines and immunotherapy.
    Journal of immunology research. 01/2014; 2014:593562.
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    ABSTRACT: The activating immunoreceptor NKG2D (natural killer group 2, member D) and its ligands play important roles in the innate and adaptive immune responses. UL16-binding protein 3 (ULBP3), an NKG2D ligand, is overexpressed on certain epithelial tumor cells. In this study, we investigated the effect of ULBP3 expression on the cytotoxic activity of natural killer (NK) cells. ULBP3 were measured by flow cytometry analysis, immunohistochemistry, and time-resolved fluoroimmunoassay. The cytotoxicity of NK cells was determined with the lactate dehydrogenase release assay. We found that ULBP3 was overexpressed on tumor cell lines and tumor tissues. Serum from cancer patients, but not from healthy donors, contained elevated levels of soluble ULBP3 (sULBP3). Importantly, high expression of ULBP3 on the cell surface of tumor cells augmented NKG2D-mediated NK cell cytotoxicity. However, low levels of sULBP3 (<15 ng/ml) weakened the cytotoxicity of NK cells by decreasing NKG2D expression on NK cells. Further analysis showed that serum samples from most cancer patients (>70%) contained the low level of sULBP3. Our results demonstrate that tumor cells express surface and soluble ULBP3, which regulate NK cell activity. Thus, ULBP3 is a potential therapeutic target for improving the immune response against cancer.
    Scientific reports. 01/2014; 4:6138.
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    ABSTRACT: Objective To investigate the expressions of let-7a and IL-6 in esophageal squamous cell carcinoma (ESCC) tissues and to analyze their correlations. Methods The expression of let-7a in tumor tissues and matched adjacent non-tumor tissues of 40 ESCC patients was detected by stem-loop RT-PCR, and the expression of IL-6 was detected by quantitative real-time PCR (qRT-PCR) and immunohistochemical staining (SP method), respectively. Results Let-7a was underexpressed in ESCC tissues compared with matched non-tumor tissues (P<0.01); IL-6 mRNA was overexpressed in ESCC tissues compared with matched non-tumor tissues (P<0.01); the positive rate of IL-6 protein in ESCC tissues was significantly higher than that in non-tumor tissues (P<0.01). There was a negative relationship between the level of let-7a and IL-6 mRNA (r=-0.974; P<0.01), and the level of let-7a in IL-6 positive expression group was lower than that in IL-6 negative expression group (P<0.05). Conclusion Let-7a is down-regulated and IL-6 is overexpressed in ESCC patients, suggesting that there is a significantly negative correlation between them.
    Xi bao yu fen zi mian yi xue za zhi = Chinese journal of cellular and molecular immunology 11/2013; 29(11):1181-4.
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    ABSTRACT: The UL16-binding proteins (ULBPs) are a novel family of human MHC class I-related, cell surface proteins that function as ligands for NKG2D. In this study, the gene encoding human ULBP3 was cloned into prokaryotic expression vector pQE30, resulting in a recombinant plasmid pQE30-ULBP3. The pQE30-ULBP3 was transformed into Escherichia coli M15 and induced the expression of recombinant protein ULBP3 (rec-ULBP3). The purified rec-ULBP3 as an antigen was used to immunize BALB/c mice. Through cell fusion, sub-cloning, and screening approach, three hybridoma cell clones expressing monoclonal antibodies (MAb) were acquired. The results from Western blot analysis, flow cytometry, and enzyme-linked immunosorbent assay showed that the hybridoma clones B2-F1-F1 and B4-C5-D11, and not G2-A4-A12, reacted with rec-ULBP3 and nature ULBP3 expressed on the cell surface of the tumor cells. In conclusion, the new MAb described here provides a valuable tool for further investigating ULBP3 function and clinical application.
    Hybridoma (2005) 06/2012; 31(3):203-8. · 0.33 Impact Factor