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Articles by S Shen
Total Records ( 6 ) for S Shen
  Y Min , W Xu , D Liu , S Shen , Y Lu , L Zhang and H. Wang

Dendritic cells (DCs) are important for the initiation of the adaptive immune response against Mycobacterium tuberculosis. Autophagy is an innate and adaptive defense mechanism and important for the control of M. tuberculosis. However, the role of autophagy in the adaptive immune response against M. tuberculosis remains to be determined. In the present study, we studied the effects of autophagy on the maturation of DCs infected with Bacillus Calmette–Guérin (BCG). The phenotype and function of the DCs were assessed by measuring the expression of CD86 and HLA-DR and the secretion of IL-10 and IL-6. Autophagy was evaluated by the change in LC3II, a molecular marker for autophagy. Following stimulation of autophagy, DCs that were matured in the presence of BCG showed enhanced expression of CD86 and HLA-DR and increased IL-6 production. The expression of LC3II was increased after the stimulation of autophagy. These results demonstrated that autophagy might result in the increased maturation of BCG-infected DCs, suggesting that autophagy could contribute to an enhanced adaptive immune response against M. tuberculosis.

  Q Guo , S Shen , M Liao , P Lian and X. Wang

Colon cancer is a common malignant tumor that is associated with increased morbidity and mortality. Nasopharyngeal carcinoma-associated gene 6 (NGX6) is a novel candidate suppressor gene of tumor metastasis, which is down-regulated in colon cancer. This study was designed to investigate the roles of NGX6 on the growth and invasiveness of human colon cancer cell line, HT-29, and to elucidate the molecular mechanism of their action. Results showed that NGX6 could inhibit the invasiveness and extracellular matrix adhesion of HT-29 cells and restore the gap junctional intercellular communication of cells. Moreover, NGX6 could suppress the translocation of β-catenin from nucleus and cytoplasm to plasma membrane, inhibit the activity of TCF4 transcript factor, and down-regulate the expression of Wnt-direct-targeted genes c-myc, cyclin D1 and COX-2. We suggested that NGX6 inhibits cell invasion and adhesion through the suppression of Wnt signal pathway in colon cancer.

  L Zhang , T Deng , X Li , H Liu , H Zhou , J Ma , M Wu , M Zhou , S Shen , Z Niu , W Zhang , L Shi , B Xiang , J Lu , L Wang , D Li , H Tang and G. Li

microRNAs (miRNAs) are small non-coding RNAs and have been implicated in the pathology of various diseases, including cancer. Here we report that the miRNA profiles have been changed after knockdown of one of the most important oncogene c-MYC or re-expression of a candidate tumor suppressor gene SPLUNC1 in nasopharyngeal carcinoma (NPC) cells. Both c-MYC knockdown and SPLUNC1 re-expression can down-regulate microRNA-141 (miR-141). miR-141 is up-regulated in NPC specimens in comparison with normal nasopharyngeal epithelium. Inhibition of miR-141 could affect cell cycle, apoptosis, cell growth, migration and invasion in NPC cells. We found that BRD3, UBAP1 and PTEN are potential targets of miR-141, which had been confirmed following luciferase reporter assays and western blotting. BRD3 and UBAP1 are both involved in NPC carcinogenesis as confirmed through our previous studies and PTEN is a crucial tumor suppressor in many tumor types. BRD3 is involved in the regulation of the Rb/E2F pathway. Inhibition of miR-141 could affect some important molecules in the Rb/E2F, JNK2 and AKT pathways. It is well known that carcinogenesis of NPC is involved in the networks of genetic and epigenetic alteration events. We propose that miR-141- and tumor-related genes c-MYC, SPLUNC1, BRD3, UBAP1 and PTEN may constitute a gene–miRNA network to contribute to NPC development.

  L Lin , P Jiang , S Shen , S Sato , B. L Davidson and Y. Xing

Transposable elements (TEs) are major sources of new exons in higher eukaryotes. Almost half of the human genome is derived from TEs, and many types of TEs have the potential to exonize. In this work, we conducted a large-scale analysis of human exons derived from mammalian-wide interspersed repeats (MIRs), a class of old TEs which was active prior to the radiation of placental mammals. Using exon array data of 328 MIR-derived exons and RT–PCR analysis of 39 exons in 10 tissues, we identified 15 constitutively spliced MIR exons, and 15 MIR exons with tissue-specific shift in splicing patterns. Analysis of RNAs from multiple species suggests that the splicing events of many strongly included MIR exons have been established before the divergence of primates and rodents, while a small percentage result from recent exonization during primate evolution. Interestingly, exon array data suggest substantially higher splicing activities of MIR exons when compared with exons derived from Alu elements, a class of primate-specific retrotransposons. This appears to be a universal difference between exons derived from young and old TEs, as it is also observed when comparing Alu exons to exons derived from LINE1 and LINE2, two other groups of old TEs. Together, this study significantly expands current knowledge about exonization of TEs. Our data imply that with sufficient evolutionary time, numerous new exons could evolve beyond the evolutionary intermediate state and contribute functional novelties to modern mammalian genomes.

  Y Chen , C Qian , C Guo , F Ge , X Zhang , X Gao , S Shen , B Lian , K Kitazato , Y Wang and S. Xiong

Nucleoside diphosphate phosphate transferase A (NDPK-A) has been shown to play critical roles in the regulation of proliferation, differentiation, growth and apoptosis of cells. Our previous study suggested that the disulphide cross-linkage between cysteine 4 (C4) and cysteine 145 (C145) of NDPK-A might be a possible regulator of its activity. To confirm this hypothesis, the C145 residue of NDPK-A was mutated to serine, and the isomerization and biological activities of the mutant were investigated and compared with those of its wild-type counterpart. It was found the C145S mutation eliminated the intramolecular disulphide bond (DB) and prevented the formation of intermolecular DB, which was known to dissociate the hexameric NDPK-A into dimeric one. We also demonstrated that the C145S mutation didn’t affect the autologous hexamerization of this protein, and the mutant had increased bioactivities including phosphate transferase and DNase. These findings support the hypothesis that the formation of DBs in NDPK-A is involved in the regulation of the oligomerization and bioactivity of this multiple function protein, and that C145 is a key residue in the regulation of NDPK-A. In addition, the C145S mutant that we have constructed might be an attractive candidate for use in applications that require NDPK-A.

  M. W.L Leung , S Shen and J. J. Lafaille

Numerous studies have highlighted the importance of high-affinity interactions between T cell receptors (TCRs) and their ligands in the selection of Foxp3+ regulatory T cells (T reg cells). To determine the role of the TCR in directing T cells into the Foxp3+ lineage, we generated transgenic (Tg) mice expressing TCRs from Foxp3+ cells. Initial analyses of the TCR Tg mice crossed with RAG-deficient mice showed that the percentage of Foxp3+ cells was very low. However, intrathymic injection and bone marrow chimera experiments showed a saturable increase of the Foxp3+ population when T reg TCR Tg cells were present in low numbers. Furthermore, when analyzing whole thymi of T reg TCR Tg RAG-deficient mice, we found significantly more Foxp3+ cells than in conventional T cell TCR Tg mice. Our results indicate that although the TCR has an instructive role in determining Foxp3 expression, selection of Foxp3+ individual clones in the thymus is limited by a very small niche.

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