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Zhang X.,Fudan University | Fei Z.,Fudan University | Wan J.,Shenzhen Medical Center | Xu J.,Fudan University | And 2 more authors.
International Journal of Immunogenetics | Year: 2011

Psoriasis is a chronic inflammatory skin disease with an immunogenetic background. This study aimed to determine the association between three functional SNPs of BANK1 (rs10516487, rs17266594 and rs3733197) with psoriasis in Southern Han Chinese population by determining their frequency in 242 patients with psoriasis and 317 healthy individuals. The genotype frequencies of the detected polymorphisms were analysed in relation to the susceptibility of psoriasis. Our data show that there is no significant difference in genotype distribution for the three BANK1 SNPs between patients and healthy controls. The AA frequency of rs3733197 is significantly higher in patients with psoriasis onset before the age of 23 than in those with late disease onset (P=0.0069). In addition, analysis on BANK1 haplotype also suggests a protective role for TGC and CAT haplotype from psoriasis (OR 0.55, 95% CI: 0.34-0.89; P=0.0144; OR 0.62, 95% CI: 0.42-0.92; P=0.0175), whereas CGT haplotype is associated with increased risk of the disease (OR 1.38, 95% CI: 1.05-1.81, P=0.0203). Overall, our result indicates that polymorphism in BANK1 is associated with susceptibility to psoriasis in Southern Han Chinese. © 2011 Blackwell Publishing Ltd. Source

Zhang T.,Shenzhen Nanshan Center for Chronic Disease Control | Lv C.,Shenzhen Nanshan Center for Chronic Disease Control | Li L.,Shenzhen Nanshan Center for Chronic Disease Control | Chen S.,Shenzhen Nanshan Center for Chronic Disease Control | And 7 more authors.
BioMed Research International | Year: 2013

Type 2 diabetes mellitus (T2DM) is a major public health problem in China. Diagnostic markers are urgently needed to identify individuals at risk of developing T2DM and encourage them to adapt to a healthier life style. Circulating miRNAs present important sources of noninvasive biomarkers of various diseases. Recently, a novel plasma microRNA signature was identified in T2DM. Here, we evaluated the T2DM-related miRNA signature in plasma of three study groups: normal (fasting glucose (FG), 4.8-5.2 mmol/L), T2DM-susceptible (FG, 6.1-6.9 mmol/L), and T2DM individuals (FG, ≥7.0 mmol/L) and tested the feasibility of using circulating miRNAs to identify individuals at risk of developing T2DM. Among the 5 miRNAs included in the signature, miR-29b and miR-28-3p are not detectable. miR-15a and miR-223 have comparable expression levels among three groups. Notably, miR-126 is the only miRNA that showed significantly reduced expression in susceptible individuals and T2DM patients compared to normal individuals, suggesting that miR-126 in circulation may serve as a potential biomarker for early identification of susceptible individuals to T2DM. © 2013 Tao Zhang et al. Source

Tang H.,Sun Yat Sen University | Wu Z.,Fudan University | Zhang J.,Jinan University | Su B.,Biomedical Research Institute | And 2 more authors.
Molecular Medicine Reports | Year: 2013

Oral squamous cell carcinoma (OSCC) is a common and lethal malignancy. Thus, improvement in current knowledge of molecular changes associated with OSCC is urgently needed to explore novel avenues of diagnostics and treatment of this disease. While aberrant expression of long non.coding RNAs (lncRNAs) has been functionally associated with certain types of cancer, including lung, breast and prostate carcinomas, their expression pattern and biological relevance in OSCC is currently unknown. In the present study, the relative abundance of a collection of lncRNAs in tissue or saliva samples from OSCC patients was investigated. It was shown that subsets of lncRNAs are expressed across non.tumor, tumor and metastatic tissue samples. Some detected lncRNAs were shown to be aberrantly expressed in cases of oral cancer and metastasis. Moreover, whole saliva contained a detectable amount of some lncRNAs, which appeared to be potential markers for OSCC. These findings suggest that the detection of lncRNAs in saliva may be used as a noninvasive and rapid diagnostic tool for the diagnosis of oral cancer. Source

Shuyi Yu.,Shenzhen Medical Center | Shuyi Yu.,Peking University | Feng W.,Peking University | Jing T.,Peking University | And 9 more authors.
Oral Surgery, Oral Medicine, Oral Pathology, Oral Radiology and Endodontology | Year: 2011

Objective: In this study, the hypothesis that hBD-3 is upregulated by LPS via epidermal growth factor receptor (EGFR) signaling pathways to enhance metastasis in oral squamous cell carcinoma (OSCC) was tested. Study design: hBD-3 expression in human tissue specimens was evaluated by RT-qPCR and immunohistochemical staining. The presence of hBD-3 peptide in the culture supernatants of each type of treated cells was evaluated by enzyme-linked immunosorbent assay. The chemotaxis response to LPS or hBD-3 protein of SCC-25 cells or siRNA-hBD-3 transfected cells were also measured by chemotaxis assay. Paired, 2-tailed Student t test and analysis of variance was used to assess the statistical significance between 2 groups or many groups. Results: hBD-3 is highly expressed and associated with lymphatic invasion of OSCC. hBD-3 expression and EGFR phosphorylation were markedly upregulated when SCC-25 cells were treated with LPS. When SCC-25 cells were preincubated with EGFR inhibitor or TLR4-neutralizing Ab before LPS stimulation, a decrease in the expression of hBD-3 was observed. hBD-3 markedly enhanced cancer metastasis, and the chemotaxis response to LPS of SCC-25 cells was partly blocked by siRNA target hBD-3. Conclusion: These findings indicate that hBD-3 is upregulated by LPS via EGFR signaling pathways to enhance lymphatic invasion of OSCC. Source

Su B.,Roswell Park Cancer Institute | Su B.,Shenzhen Medical Center | Gao L.,Roswell Park Cancer Institute | Meng F.,State University of New York at Buffalo | And 3 more authors.
Oncogene | Year: 2013

Metastatic cell migration and invasion are regulated by altered adhesion-mediated signaling to the actin-based cytoskeleton via activated Src-FAK complexes. Src-suppressed C-kinase substrate (SSeCKS, the rodent orthologue of human Gravin/AKAP12), whose expression is downregulated by oncogenic Src and in many human cancers, antagonizes oncogenic Src pathways including those driving neovascularization at metastatic sites, metastatic cell motility and invasiveness. This is likely manifested through its function as a scaffolder of F-actin and signaling proteins such as cyclins, calmodulin, protein kinase C and A. Here we show that in contrast to its ability to inhibit haptotaxis, SSeCKS increased prostate cancer cell adhesion to fibronectin and type I collagen in a FAK-dependent manner, correlating with a relative increase in FAK poY397 levels. In contrast, SSeCKS suppressed adhesion-induced Src activation (Src poY416) and phosphorylation of FAK at Y925, a known Src substrate site. SSeCKS also induced increased cell spreading, cell flattening, integrin β1 clustering and formation of mature focal adhesion plaques. An in silico analysis identified a Src-binding domain on SSeCKS(aa 153-166) that is homologous to the Src-binding domain of caveolin-1, and this region is required for SSeCKS-Src interaction, for SSeCKS-enhanced Src activity and sequestration to lipid rafts and for SSeCKS-enhanced adhesion of MAT-LyLu and CWR22Rv1 prostate cancer cells. Our data suggest a model in which SSeCKS suppresses oncogenic motility by sequestering Src to caveolin-rich lipid rafts, thereby disengaging Src from FAK-associated adhesion and signaling complexes. © 2013 Macmillan Publishers Limited All rights reserved. Source

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